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1
Dean, J. B., and J. A. Boulant. "Delayed firing rate responses to temperature in diencephalic slices." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 3 (September 1, 1992): R679—R684. http://dx.doi.org/10.1152/ajpregu.1992.263.3.r679.
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Thermoregulatory responses may be delayed in onset and offset by several minutes after changes in hypothalamic temperature. Our preceding study found neurons that displayed delayed firing rate responses during clamped thermal stimulation in remote regions of rat diencephalic tissue slices. The present study looked for similar delayed firing rate responses during clamped (1.5-10 min) changes in each neuron's local temperature. Of 26 neurons tested with clamped thermal stimulation, six (i.e., 23%) showed delayed responses, with on-latencies of 1.0-7.8 min. These neurons rarely showed off-latencies, and the delayed response was not eliminated by synaptic blockade. The on-latencies and ranges of local thermosensitivity were similar to delayed neuronal responses to remote temperature; however, remote-sensitive neurons displayed off-latencies, higher firing rates at 37 degrees C, and greater sensitivity to thermal stimulation. Our findings suggest that delayed thermosensitivity is an intrinsic property of certain neurons and may initiate more elaborate or prolonged delayed responses in synaptically connected diencephalic networks. These networks could explain the delayed thermoregulatory responses observed during hypothalamic thermal stimulation.
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RIND, F. CLAIRE. "IDENTIFICATION OF DIRECTIONALLY SELECTIVE MOTION-DETECTING NEURONES IN THE LOCUST LOBULA AND THEIR SYNAPTIC CONNECTIONS WITH AN IDENTIFIED DESCENDING NEURONE." Journal of Experimental Biology 149, no. 1 (March 1, 1990): 21–43. http://dx.doi.org/10.1242/jeb.149.1.21.
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The anatomy and physiology of two directionally selective motion-detecting neurones in the locust are described. Both neurones had dendrites in the lobula, and projected to the ipsilateral protocerebrum. Their cell bodies were located on the posterio-dorsal junction of the optic lobe with the protocerebrum. The neurones were sensitive to horizontal motion of a visual stimulus. One neurone, LDSMD(F), had a preferred direction forwards over the ipsilateral eye, and a null direction backwards. The other neurone, LDSMD(B), had a preferred direction backwards over the ipsilateral eye 1. Motion in the preferred direction caused EPSPs and spikes in the LDSMD neurones. Motion in the null direction resulted in IPSPs 2. Both excitatory and inhibitory inputs were derived from the ipsilateral eye 3. The DSMD neurones responded to velocities of movement up to and beyond 270°s−1 4. The response of both LDSMD neurones showed no evidence of adaptation during maintained apparent or real movement 5. There was a delay of 60–80 ms between a single step of apparent movement, either the preferred or the null direction, and the start of the response 6. There was a monosynaptic, excitatory connection between the LDSMD(B) neurone and the protocerebral, descending DSMD neurone (PDDSMD) identified in the preceding paper (Rind, 1990). At resting membrane potential, a single presynaptic spike did not give rise to a spike in the postsynaptic neurone
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SONG, YUNING, and CURTIS L. BAKER. "Neural mechanisms mediating responses to abutting gratings: Luminance edgesvs.illusory contours." Visual Neuroscience 23, no. 2 (March 2006): 181–99. http://dx.doi.org/10.1017/s0952523806232036.
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The discontinuities of phase-shifted abutting line gratings give rise to perception of an “illusory contour” (IC) along the line terminations. Neuronal responses to such ICs have been interpreted as evidence for a specialized visual mechanism, since such responses cannot be predicted from conventional linear receptive fields. However, when the spatial scale of the component gratings (carriers) is large compared to the neuron's luminance passband, these IC responses might be evoked simply by the luminance edges at the line terminations. Thus by presenting abutting gratings at a series of carrier spatial scales to cat A18 neurons, we were able to distinguish genuine nonlinear responses from those due to luminance edges. Around half of the neurons (both simple and complex types) showed a bimodal response pattern to abutting gratings: one peak at a low carrier spatial frequency range that overlapped with the luminance passband, and a second distinct peak at much higher frequencies beyond the neuron's grating resolution. For those bimodally responding neurons, the low-frequency responses were sensitive to carrier phase, but the high-frequency responses were phase-invariant. Thus the responses at low carrier spatial frequencies could be understoodviaa linear model, while the higher frequency responses represented genuine nonlinear IC processing. IC responsive neurons also demonstrated somewhat lower spatial preference to the periodic contours (envelopes) compared to gratings, but the optimal orientation and motion direction for both were quite similar. The nonlinear responses to ICs could be explained by the same energy mechanism underlying responses to second-order stimuli such as contrast-modulated gratings. Similar neuronal preferences for ICs and for gratings may contribute to the form-cue invariant perception of moving contours.
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Karmeier, K., J. H. van Hateren, R. Kern, and M. Egelhaaf. "Encoding of Naturalistic Optic Flow by a Population of Blowfly Motion-Sensitive Neurons." Journal of Neurophysiology 96, no. 3 (September 2006): 1602–14. http://dx.doi.org/10.1152/jn.00023.2006.
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In sensory systems information is encoded by the activity of populations of neurons. To analyze the coding properties of neuronal populations sensory stimuli have usually been used that were much simpler than those encountered in real life. It has been possible only recently to stimulate visual interneurons of the blowfly with naturalistic visual stimuli reconstructed from eye movements measured during free flight. Therefore we now investigate with naturalistic optic flow the coding properties of a small neuronal population of identified visual interneurons in the blowfly, the so-called VS and HS neurons. These neurons are motion sensitive and directionally selective and are assumed to extract information about the animal's self-motion from optic flow. We could show that neuronal responses of VS and HS neurons are mainly shaped by the characteristic dynamical properties of the fly's saccadic flight and gaze strategy. Individual neurons encode information about both the rotational and the translational components of the animal's self-motion. Thus the information carried by individual neurons is ambiguous. The ambiguities can be reduced by considering neuronal population activity. The joint responses of different subpopulations of VS and HS neurons can provide unambiguous information about the three rotational and the three translational components of the animal's self-motion and also, indirectly, about the three-dimensional layout of the environment.
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Thompson, Gregory W., Magda Horackova, and J. Andrew Armour. "Sensitivity of canine intrinsic cardiac neurons to H2O2and hydroxyl radical." American Journal of Physiology-Heart and Circulatory Physiology 275, no. 4 (October 1, 1998): H1434—H1440. http://dx.doi.org/10.1152/ajpheart.1998.275.4.h1434.
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To determine whether intrinsic cardiac neurons are sensitive to oxygen-derived free radicals in situ, studies were performed in 44 open-chest anesthetized dogs. 1) When H2O2(600 μM) was administered to right atrial neurons of 36 dogs via their local arterial blood supply, neuronal activity either increased (+92% in 16 dogs) or decreased (−61% in 20 dogs), depending on the population of neurons studied. H2O2(600 μM) administered into the systemic circulation did not affect neuronal activity, measured cardiac indexes, or aortic pressure. 2) The iron-chelating agent deferoxamine (20 mg/kg iv), a chemical that prevents the formation of oxygen-derived free radicals, reduced the activity generated by neurons (−57%) in 8 of 10 dogs. 3) H2O2did not affect neuronal activity when administered in the presence of deferoxamine in these 10 dogs. 4) When the ATP-sensitive potassium (KATP) channel opener cromakalim (20 μM) was administered to intrinsic cardiac neurons in another 21 animals via their regional arterial blood supply, ongoing neuronal activity in 15 of these dogs decreased by 54%. 5) Neuronal activity was not affected by H2O2when administered in the presence of cromakalim in 16 dogs. These data indicate that 1) some intrinsic cardiac neurons are sensitive to exogenous H2O2, 2) such neurons are tonically influenced by locally produced oxygen-derived free radicals in situ, and 3) intrinsic cardiac neurons possess KATPchannels that are functionally important during oxidative challenge.
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Inokuchi, A., Y. Oomura, N. Shimizu, and T. Yamamoto. "Central action of glucagon in rat hypothalamus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 1 (January 1, 1986): R120—R126. http://dx.doi.org/10.1152/ajpregu.1986.250.1.r120.
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The effects of electrophoretically applied glucagon on neuronal activity in the rat lateral hypothalamic area (LHA), dorsomedial hypothalamic nucleus (DMH), and ventromedial hypothalamic nucleus (VMH) were examined. In the LHA glucagon significantly suppressed the activity of glucose-sensitive neurons compared with its effect on non-glucose-sensitive neurons. This inhibitory effect of glucagon on LHA neurons was blocked by ouabain. Intracellular recordings from LHA neurons revealed that glucagon hyperpolarized the cell membrane without a significant change in the input membrane resistance. Intra-arterial injection of glucagon suppressed the activity of some neurons that were suppressed by electrophoretically applied glucagon. Similarly, glucagon suppressed the activity of significant numbers of DMH and VMH neurons with doses higher than those that affected LHA glucose-sensitive neurons. Cortical neurons were unaffected by glucagon. The data suggest that blood-borne glucagon could suppress the activity of LHA glucose-sensitive neurons and, in addition, might contribute to the control of metabolism and the termination of feeding behavior.
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Kanda, Shinji, Yasuhisa Akazome, Takuya Matsunaga, Naoyuki Yamamoto, Shunji Yamada, Hiroko Tsukamura, Kei-ichiro Maeda, and Yoshitaka Oka. "Identification of KiSS-1 Product Kisspeptin and Steroid-Sensitive Sexually Dimorphic Kisspeptin Neurons in Medaka (Oryzias latipes)." Endocrinology 149, no. 5 (January 17, 2008): 2467–76. http://dx.doi.org/10.1210/en.2007-1503.
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Recently, a novel physiologically active peptide, kisspeptin (metastin), has been reported to facilitate sexual maturation and ovulation by directly stimulating GnRH neurons in several mammalian species. Despite its importance in the neuroendocrine regulation of reproduction, kisspeptin neurons have only been studied in mammals, and there has been no report on the kisspeptin or kisspeptin neuronal systems in nonmammalian vertebrates. We used medaka for the initial identification of the KiSS-1 gene and the anatomical distribution of KiSS-1 mRNA expressing neurons (KiSS-1 neurons) in the brain of nonmammalian species. In situ hybridization for the medaka KiSS-1 gene cloned here proved that two kisspeptin neuronal populations are localized in the hypothalamic nuclei, the nucleus posterioris periventricularis and the nucleus ventral tuberis (NVT). Furthermore, NVT KiSS-1 neurons were sexually dimorphic in number (male neurons ≫ female neurons) under the breeding conditions. We also found that the number of KiSS-1 neurons in the NVT but not that in the nucleus posterioris periventricularis was positively regulated by ovarian estrogens. The fact that there were clear differences in the number of NVT KiSS-1 neurons between the fish under the breeding and nonbreeding conditions strongly suggests that the steroid-sensitive changes in the KiSS-1 mRNA expression in the NVT occur physiologically, according to the changes in the reproductive state. From the present results, we conclude that the medaka KiSS-1 neuronal system is involved in the central regulation of reproductive functions, and, given many experimental advantages, the medaka brain may serve as a good model system to study its physiology.
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Dogas, Z., M. Krolo, E. A. Stuth, M. Tonkovic-Capin, F. A. Hopp, D. R. McCrimmon, and E. J. Zuperku. "Differential Effects of GABAA Receptor Antagonists in the Control of Respiratory Neuronal Discharge Patterns." Journal of Neurophysiology 80, no. 5 (November 1, 1998): 2368–77. http://dx.doi.org/10.1152/jn.1998.80.5.2368.
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Dogas, Z., M. Krolo, E. A. Stuth, M. Tonkovic-Capin, F. A. Hopp, D. R. McCrimmon, and E. J. Zuperku. Differential effects of GABAA receptor antagonists in the control of respiratory neuronal discharge patterns. J. Neurophysiol. 80: 2368–2377, 1998. To ascertain the role of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) in shaping and controlling the phasic discharge patterns of medullary respiratory premotor neurons, localized pressure applications of the competitive GABAA receptor antagonist bicuculline (BIC) and the noncompetitive GABAA receptor antagonist picrotoxin (PIC) were studied. Multibarrel micropipettes were used in halothane anesthetized, paralyzed, ventilated, vagotomized dogs to record single unit activity from inspiratory and expiratory neurons in the caudal ventral respiratory group and to picoeject GABAA receptor antagonists. The moving time average of phrenic nerve activity was used to determine respiratory phase durations and to synchronize cycle-triggered histograms of discharge patterns. Picoejection of BIC and PIC had qualitatively different effects on the discharge patterns of respiratory neurons. BIC caused an increase in the discharge rate during the neuron's active phase without inducing activity during the neuron's normally silent phase. The resulting discharge patterns were amplified replicas (×2–3) of the underlying preejection phasic patterns. In contrast, picoejection of PIC did not increase the peak discharge rate during the neuron's active phase but induced a tonic level of activity during the neuron's normally silent phase. The maximum effective BIC dose (15 ± 1.8 pmol/min) was considerably smaller than that for PIC (280 ± 53 pmol/min). These findings suggest that GABAA receptors with differential pharmacology mediate distinct functions within the same neuron, 1) gain modulation that is BIC sensitive but PIC insensitive and 2) silent-phase inhibition blocked by PIC. These studies also suggest that the choice of an antagonist is an important consideration in the determination of GABA receptor function within the respiratory motor control system.
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Zhang, Tao, and Kenneth H. Britten. "The Responses of VIP Neurons Are Sufficiently Sensitive to Support Heading Judgments." Journal of Neurophysiology 103, no. 4 (April 2010): 1865–73. http://dx.doi.org/10.1152/jn.00401.2009.
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The ventral intraparietal area (VIP) of the macaque monkey is thought to be involved in judging heading direction based on optic flow. We recorded neuronal discharges in VIP while monkeys were performing a two-alternative, forced-choice heading discrimination task to relate quantitatively the activity of VIP neurons to monkeys' perceptual choices. Most VIP neurons were responsive to simulated heading stimuli and were tuned such that their responses changed across a range of forward trajectories. Using receiver operating characteristic (ROC) analysis, we found that most VIP neurons were less sensitive to small heading changes than was the monkey, although a minority of neurons were equally sensitive. Pursuit eye movements modestly yet significantly increased both neuronal and behavioral thresholds by approximately the same amount. Our results support the view that VIP activity is involved in self-motion judgments.
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Aggarwal, Sanya, Celion Tang, Kristen Sing, Hyun Wook Kim, Robert P. Millar, and Javier A. Tello. "Medial Amygdala Kiss1 Neurons Mediate Female Pheromone Stimulation of Luteinizing Hormone in Male Mice." Neuroendocrinology 108, no. 3 (December 10, 2018): 172–89. http://dx.doi.org/10.1159/000496106.
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Background/Aims: The medial amygdala (MeA) responds to olfactory stimuli and alters reproductive physiology. However, the neuronal circuit that relays signals from the MeA to the reproductive axis remains poorly defined. This study aimed to test whether MeA kisspeptin (MeAKiss) neurons in male mice are sensitive to sexually relevant olfactory stimuli and transmit signals to alter reproductive physiology. We also investigated whether MeAKiss neurons have the capacity to elaborate glutamate and GABA neurotransmitters and potentially contribute to reproductive axis regulation. Methods: Using female urine as a pheromone stimulus, MeAKiss neuronal activity was analysed and serum luteinizing hormone (LH) was measured in male mice. Next, using a chemogenetic approach, MeAKiss neurons were bi-directionally modulated to measure the effect on serum LH and evaluate the activation of the preoptic area. Lastly, using in situ hybridization, we identified the proportion of MeAKiss neurons that express markers for GABAergic (Vgat) and glutamatergic (Vglut2) neurotransmission. Results: Male mice exposed to female urine showed a two-fold increase in the number of c-Fos-positive MeAKiss neurons concomitant with raised LH. Chemogenetic activation of MeAKiss neurons significantly increased LH in the absence of urine exposure, whereas inhibition of MeAKiss neurons did not alter LH. In situ hybridization revealed that MeAKiss neurons are a mixed neuronal population in which 71% express Vgat mRNA, 29% express Vglut2 mRNA, and 6% express both. Conclusions: Our results uncover, for the first time, that MeAKiss neurons process sexually relevant olfactory signals to influence reproductive hormone levels in male mice, likely through a complex interplay of neuropeptide and neurotransmitter signalling.
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Zhang, Weirong, Flávia R. Carreño, J. Thomas Cunningham, and Steve W. Mifflin. "Chronic sustained and intermittent hypoxia reduce function of ATP-sensitive potassium channels in nucleus of the solitary tract." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 5 (November 2008): R1555—R1562. http://dx.doi.org/10.1152/ajpregu.90390.2008.
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Activation of neuronal ATP-sensitive potassium (KATP) channels is an important mechanism that protects neurons and conserves neural function during hypoxia. We investigated hypoxia (bath gassed with 95% N2-5% CO2 vs. 95% O2-5% CO2 in control)-induced changes in KATP current in second-order neurons of peripheral chemoreceptors in the nucleus of the solitary tract (NTS). Hypoxia-induced KATP currents were compared between normoxic (Norm) rats and rats exposed to 1 wk of either chronic sustained hypoxia (CSH) or chronic intermittent hypoxia (CIH). Whole cell recordings of NTS second-order neurons identified after 4-(4-(dihexadecylamino)styryl)- N-methylpyridinium iodide (DiA) labeling of the carotid bodies were obtained in a brain stem slice. In Norm cells ( n = 9), hypoxia (3 min) induced an outward current of 12.7 ± 1.1 pA with a reversal potential of −73 ± 2 mV. This current was completely blocked by the KATP channel blocker tolbutamide (100 μM). Bath application of the KATP channel opener diazoxide (200 μM, 3 min) evoked an outward current of 21.8 ± 5.8 pA ( n = 6). Hypoxia elicited a significantly smaller outward current in both CSH (5.9 ± 1.4 pA, n = 11; P < 0.01) and CIH (6.8 ± 1.7 pA, n = 6; P < 0.05) neurons. Diazoxide elicited a significantly smaller outward current in CSH (3.9 ± 1.0 pA, n = 5; P < 0.05) and CIH (2.9 ± 0.9 pA, n = 3; P < 0.05) neurons. Western blot analysis showed reduced levels of KATP potassium channel subunits Kir6.1 and Kir6.2 in the NTS from CSH and CIH rats. These results suggest that hypoxia activates KATP channels in NTS neurons receiving monosynaptic chemoreceptor afferent inputs. Chronic exposure to either sustained or intermittent hypoxia reduces KATP channel function in NTS neurons. This may represent a neuronal adaptation that preserves neuronal excitability in crucial relay neurons in peripheral chemoreflex pathways.
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Ritter, R. C., S. Ritter, W. R. Ewart, and D. L. Wingate. "Capsaicin attenuates hindbrain neuron responses to circulating cholecystokinin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 5 (November 1, 1989): R1162—R1168. http://dx.doi.org/10.1152/ajpregu.1989.257.5.r1162.
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Capsaicin is a neurotoxin that destroys small sensory neurons with unmyelinated axons, including a subpopulation of vagal sensory neurons. Capsaicin treatment attenuates suppression of food intake induced by systemic administration of cholecystokinin (CCK) but not by gastric distension. However, both gastric distension and intravascular CCK alter the discharge of dorsal hindbrain neurons by a vagal mechanism. Therefore, it is plausible that some hindbrain neurons receive convergent input from capsaicin-sensitive vagal neurons that are responsive to CCK and also from capsaicin-insensitive neurons that are responsive to gastric distension. To investigate this possibility we made extracellular recordings from gastric distension-responsive hindbrain neurons during intra-arterial cholecystokinin octapeptide (CCK-8) administration in anesthetized intact and capsaicin-pretreated rats. We found that capsaicin-pretreated rats exhibit attenuated neuronal discharge responses to CCK-8 but not to gastric distension. These results are consistent with the existence of convergent CCK-sensitive and gastric distension-sensitive afferent inputs to hindbrain neurons and suggest that various gastrointestinal sensory modalities may be communicated to the brain by populations of neurons that can be distinguished by their sensitivity to neurotoxins.
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Travis, K. A., and J. A. Boulant. "In vitro diencephalic neuronal thermosensitivity in normotensive and hypertensive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 2 (February 1, 1989): R560—R566. http://dx.doi.org/10.1152/ajpregu.1989.256.2.r560.
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Because morphological differences exist in hypothalamic neurons from spontaneously hypertensive (SH) and normotensive Wistar-Kyoto (WKY) rats, the present study recorded neuronal spontaneous activity and thermosensitivity from diencephalic tissue slices of these two strains. With the use of extracellular recordings from horizontal tissue slices, neurons were characterized according to location, firing rate at 37 degrees C, and firing rate response to changes in local tissue temperature. Compared with WKY neurons, SH neurons had higher firing rates in the preoptic-anterior hypothalamus and lower firing rates in the dorsomedial hypothalamus. In addition, SH warm-sensitive neurons were less thermosensitive over the hyperthermic range (37-40 degrees C), and SH temperature-insensitive neurons had higher spontaneous firing rates. These differences in spontaneous activity and thermosensitivity provide a neuronal basis to explain the elevation of core temperature observed in SH rats.
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Funke, Frank, Mathias Dutschmann, and Michael Müller. "Imaging of respiratory-related population activity with single-cell resolution." American Journal of Physiology-Cell Physiology 292, no. 1 (January 2007): C508—C516. http://dx.doi.org/10.1152/ajpcell.00253.2006.
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The pre-Bötzinger complex (PBC) in the rostral ventrolateral medulla contains a kernel involved in respiratory rhythm generation. So far, its respiratory activity has been analyzed predominantly by electrophysiological approaches. Recent advances in fluorescence imaging now allow for the visualization of neuronal population activity in rhythmogenic networks. In the respiratory network, voltage-sensitive dyes have been used mainly, so far, but their low sensitivity prevents an analysis of activity patterns of single neurons during rhythmogenesis. We now have succeeded in using more sensitive Ca2+ imaging to study respiratory neurons in rhythmically active brain stem slices of neonatal rats. For the visualization of neuronal activity, fluo-3 was suited best in terms of neuronal specificity, minimized background fluorescence, and response magnitude. The tissue penetration of fluo-3 was improved by hyperosmolar treatment (100 mM mannitol) during dye loading. Rhythmic population activity was imaged with single-cell resolution using a sensitive charge-coupled device camera and a ×20 objective, and it was correlated with extracellularly recorded mass activity of the contralateral PBC. Correlated optical neuronal activity was obvious online in 29% of slices. Rhythmic neurons located deeper became detectable during offline image processing. Based on their activity patterns, 74% of rhythmic neurons were classified as inspiratory and 26% as expiratory neurons. Our approach is well suited to visualize and correlate the activity of several single cells with respiratory network activity. We demonstrate that neuronal synchronization and possibly even network configurations can be analyzed in a noninvasive approach with single-cell resolution and at frame rates currently not reached by most scanning-based imaging techniques.
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Siveke, Ida, Christian Leibold, and Benedikt Grothe. "Spectral Composition of Concurrent Noise Affects Neuronal Sensitivity to Interaural Time Differences of Tones in the Dorsal Nucleus of the Lateral Lemniscus." Journal of Neurophysiology 98, no. 5 (November 2007): 2705–15. http://dx.doi.org/10.1152/jn.00275.2007.
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We are regularly exposed to several concurrent sounds, producing a mixture of binaural cues. The neuronal mechanisms underlying the localization of concurrent sounds are not well understood. The major binaural cues for localizing low-frequency sounds in the horizontal plane are interaural time differences (ITDs). Auditory brain stem neurons encode ITDs by firing maximally in response to “favorable” ITDs and weakly or not at all in response to “unfavorable” ITDs. We recorded from ITD-sensitive neurons in the dorsal nucleus of the lateral lemniscus (DNLL) while presenting pure tones at different ITDs embedded in noise. We found that increasing levels of concurrent white noise suppressed the maximal response rate to tones with favorable ITDs and slightly enhanced the response rate to tones with unfavorable ITDs. Nevertheless, most of the neurons maintained ITD sensitivity to tones even for noise intensities equal to that of the tone. Using concurrent noise with a spectral composition in which the neuron's excitatory frequencies are omitted reduced the maximal response similar to that obtained with concurrent white noise. This finding indicates that the decrease of the maximal rate is mediated by suppressive cross-frequency interactions, which we also observed during monaural stimulation with additional white noise. In contrast, the enhancement of the firing rate to tones at unfavorable ITD might be due to early binaural interactions (e.g., at the level of the superior olive). A simple simulation corroborates this interpretation. Taken together, these findings suggest that the spectral composition of a concurrent sound strongly influences the spatial processing of ITD-sensitive DNLL neurons.
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Kuhn, Bernd, Federico Picollo, Valentina Carabelli, and Giorgio Rispoli. "Advanced real-time recordings of neuronal activity with tailored patch pipettes, diamond multi-electrode arrays and electrochromic voltage-sensitive dyes." Pflügers Archiv - European Journal of Physiology 473, no. 1 (October 13, 2020): 15–36. http://dx.doi.org/10.1007/s00424-020-02472-4.
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AbstractTo understand the working principles of the nervous system is key to figure out its electrical activity and how this activity spreads along the neuronal network. It is therefore crucial to develop advanced techniques aimed to record in real time the electrical activity, from compartments of single neurons to populations of neurons, to understand how higher functions emerge from coordinated activity. To record from single neurons, a technique will be presented to fabricate patch pipettes able to seal on any membrane with a single glass type and whose shanks can be widened as desired. This dramatically reduces access resistance during whole-cell recording allowing fast intracellular and, if required, extracellular perfusion. To simultaneously record from many neurons, biocompatible probes will be described employing multi-electrodes made with novel technologies, based on diamond substrates. These probes also allow to synchronously record exocytosis and neuronal excitability and to stimulate neurons. Finally, to achieve even higher spatial resolution, it will be shown how voltage imaging, employing fast voltage-sensitive dyes and two-photon microscopy, is able to sample voltage oscillations in the brain spatially resolved and voltage changes in dendrites of single neurons at millisecond and micrometre resolution in awake animals.
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Boulant, J. A., and N. L. Silva. "Interactions of reproductive steroids, osmotic pressure, and glucose on thermosensitive neurons in preoptic tissue slices." Canadian Journal of Physiology and Pharmacology 65, no. 6 (June 1, 1987): 1267–73. http://dx.doi.org/10.1139/y87-202.
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The preoptic area contains thermosensitive neurons, thought to be important in thermoregulation, and steroid-sensitive neurons, thought to be involved in reproduction. The preoptic area also contains osmosensitive neurons, considered important in water balance, and glucosensitive neurons, thought to function in the regulation of glucose. If these various neurons belong to separate populations, one might predict that most osmosensitive, glucosensitive, and steroid-sensitive neurons constitute the population of temperature-insensitive neurons rather than thermosensitive neurons. To test this hypothesis, single unit activity was recorded in preoptic tissue slices prepared from male rats. In addition to temperature changes, neuronal responses were examined with various perfusion media containing testosterone or estradiol (30 pg/mL), low glucose (1.0 mM), and increased osmotic pressure (309 mosmol/kg). It was found that the steroid-sensitive, osmosensitive, and glucosensitive neurons were not confined to the temperature-insensitive neurons; but that nearly half of the thermosensitive neurons responded to these nonthermal stimuli. This lack of specificity was also observed between osmosensitive and glucosensitive neurons; however, most of the steroid-sensitive neurons were highly specific for either estradiol or testosterone. Although these findings do not suggest a strong functional specificity for preoptic neurons, they do support studies emphasizing interactions between regulatory systems.
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Zhang, Xueguo, Ronald Fogel, and William E. Renehan. "Stimulation of the paraventricular nucleus modulates the activity of gut-sensitive neurons in the vagal complex." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 1 (July 1, 1999): G79—G90. http://dx.doi.org/10.1152/ajpgi.1999.277.1.g79.
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There is good evidence that stimulation of the lateral hypothalamus excites neurons in the dorsal vagal complex (DVC), but the data regarding the role of the paraventricular nucleus (PVN) in vagal function are less clear. The purpose of this study was to clarify the effect of PVN stimulation on the activity of neurons in the DVC. We utilized extracellular and intracellular neuronal recordings with intracellular injections of a neuronal tracer to label individual, physiologically characterized neurons in the DVC of rats anesthetized with pentobarbital sodium. Most (80%) of the gut-sensitive dorsal motor nucleus of the vagus (DMNV) neurons characterized in this study exhibited a change in activity during electrical stimulation of the PVN. Stimulation of the PVN caused an increase in the spontaneous activity of 59% of the PVN-sensitive DMNV neurons, and the PVN was capable of modulating the response of a small subset of DMNV neurons to gastrointestinal stimuli. This study also demonstrated that the PVN was capable of influencing the activity of neurons in the nucleus of the solitary tract (NST). Electrical stimulation of the PVN decreased the basal activity of 66% of the NST cells that we characterized and altered the gastrointestinal response of a very small subset of NST neurons. It is likely that these interactions play a role in the modulation of a number of gut-related homeostatic processes. Increased or decreased activity in the descending pathway from the PVN to the DVC has the potential to alter ascending satiety signals, modulate vago-vagal reflexes and the cephalic phase of feeding, and affect the absorption of nutrients from the gastrointestinal tract.
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Labhart, T. "How polarization-sensitive interneurones of crickets see the polarization pattern of the sky: a field study with an opto-electronic model neurone." Journal of Experimental Biology 202, no. 7 (April 1, 1999): 757–70. http://dx.doi.org/10.1242/jeb.202.7.757.
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Many insects gain directional information from the polarization pattern of the sky. Polarization vision is mediated by the specialized ommatidia of the dorsal rim area of the compound eye, which contains highly polarization-sensitive photoreceptors. In crickets Gryllus campestris, polarized light information conveyed by the dorsal rim ommatidia was found to be processed by polarization-opponent interneurones (POL-neurones). In this study, a field-proof opto-electronic model of a POL-neurone was constructed that implements the physiological properties of cricket POL-neurones as measured by previous electrophysiological experiments in the laboratory. Using this model neurone, both the strength of the celestial polarization signal and the directional information available to POL-neurones were assessed under a variety of meteorological conditions. We show that the polarization signal as experienced by cricket POL-neurones is very robust, both because of the special filtering properties of these neurones (polarization-antagonism, spatial low-pass, monochromacy) and because of the relatively stable e-vector pattern of the sky.
20
Geerling, Joel C., and Arthur D. Loewy. "Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 3 (March 2007): R1338—R1348. http://dx.doi.org/10.1152/ajpregu.00391.2006.
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Thirst and sodium appetite are both critical for restoring blood volume. Because these two behavioral drives can arise under similar physiological conditions, some of the brain sensory sites that stimulate thirst may also drive sodium appetite. However, the physiological and temporal dynamics of these two appetites exhibit clear differences, suggesting that they involve separate brain circuits. Unlike thirst-associated sensory neurons in the hypothalamus, the 11-β-hydroxysteroid dehydrogenase type 2 (HSD2) neurons in the rat nucleus tractus solitarius (NTS) are activated in close association with sodium appetite ( 16 ). Here, we tested whether the HSD2 neurons are also activated in response to either of the two physiological stimuli for thirst: hyperosmolarity and hypovolemia. Hyperosmolarity, produced by intraperitoneal injection of hypertonic saline, stimulated a large increase in water intake and a substantial increase in immunoreactivity for the neuronal activity marker c-Fos within the medial NTS, but not in the HSD2 neurons. Hypovolemia, produced by subcutaneous injection of hyperoncotic polyethylene glycol (PEG), stimulated an increase in water intake within 1–4 h without elevating c-Fos expression in the HSD2 neurons. The HSD2 neurons were, however, activated by prolonged hypovolemia, which also stimulated sodium appetite. Twelve hours after PEG was injected in rats that had been sodium deprived for 4 days, the HSD2 neurons showed a consistent increase in c-Fos immunoreactivity. In summary, the HSD2 neurons are activated specifically in association with sodium appetite and appear not to function in thirst.
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Sun, Hong-Shuo, Zhong-Ping Feng, Takashi Miki, Susumu Seino, and Robert J. French. "Enhanced Neuronal Damage After Ischemic Insults in Mice Lacking Kir6.2-Containing ATP-Sensitive K+ Channels." Journal of Neurophysiology 95, no. 4 (April 2006): 2590–601. http://dx.doi.org/10.1152/jn.00970.2005.
Full textAbstract:
Adenosine triphosphate (ATP)–sensitive potassium (KATP) channels, incorporating Kir6.x and sulfonylurea receptor subunits, are weak inward rectifiers that are thought to play a role in neuronal protection from ischemic insults. However, the involvement of Kir6.2-containing KATP channel in hippocampus and neocortex has not been tested directly. To delineate the physiological roles of Kir6.2 channels in the CNS, we used knockout (KO) mice that do not express Kir6.2. Immunocytochemical staining demonstrated that Kir6.2 protein was expressed robustly in hippocampal neurons of the wild-type (WT) mice and absent in the KO. To examine neuronal sensitivity to metabolic stress in vitro, and to ischemia in vivo, we 1) exposed hippocampal slices to transient oxygen and glucose deprivation (OGD) and 2) produced focal cerebral ischemia by middle cerebral artery occlusion (MCAO). Both slice and whole animal studies showed that neurons from the KO mice were severely damaged after anoxia or ischemia, whereas few injured neurons were observed in the WT, suggesting that Kir6.2 channels are necessary to protect neurons from ischemic insults. Membrane potential recordings from the WT CA1 pyramidal neurons showed a biphasic response to OGD; a brief hyperpolarization was followed by a small depolarization during OGD, with complete recovery within 30 min after returning to normoxic conditions. By contrast, CA1 pyramidal neurons from the KO mice were irreversibly depolarized by OGD exposure, without any preceding hyperpolarization. These data suggest that expression of Kir6.2 channels prevents prolonged depolarization of neurons resulting from acute hypoxic or ischemic insults, and thus protects these central neurons from the injury.
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Nakagawa, Hideki, and Kang Hongjian. "Collision-Sensitive Neurons in the Optic Tectum of the Bullfrog, Rana catesbeiana." Journal of Neurophysiology 104, no. 5 (November 2010): 2487–99. http://dx.doi.org/10.1152/jn.01055.2009.
Full textAbstract:
In this study, we examined the neuronal correlates of frog collision avoidance behavior. Single unit recordings in the optic tectum showed that 11 neurons gave selective responses to objects approaching on a direct collision course. The collision-sensitive neurons exhibited extremely tight tuning for collision bound trajectories with mean half-width at half height values of 0.8 and 0.9° ( n = 4) for horizontal and vertical deviations, respectively. The response of frog collision-sensitive neurons can be fitted by a function that simply multiplies the size dependence of its response, e−αθ( t), by the image's instantaneous angular velocity θ′( t). Using fitting analysis, we showed that the peak firing rate always occurred after the approaching object had reached a constant visual angle of 24.2 ± 2.6° (mean ± SD; n = 8), regardless of the approaching velocity. Moreover, a linear relationship was demonstrated between parameters l/v ( l: object's half-size, v: approach velocity) and time-to-collision (time difference between peak neuronal activity and the predicted collision) in the 11 collision-sensitive neurons. In addition, linear regression analysis was used to show that peak firing rate always occurred after the object had reached a constant angular size of 21.1° on the retina. The angular thresholds revealed by both theoretical analyses were comparable and showed a good agreement with that revealed by our previous behavioral experiments. This strongly suggests that the collision-sensitive neurons of the frog comprise a threshold detector, which triggers collision avoidance behavior.
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Sartor, Daniela M., Arthur Shulkes, and Anthony J. M. Verberne. "An enteric signal regulates putative gastrointestinal presympathetic vasomotor neurons in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 3 (March 2006): R625—R633. http://dx.doi.org/10.1152/ajpregu.00639.2005.
Full textAbstract:
Ingestion of a meal results in gastrointestinal (GI) hyperemia and is associated with systemic and paracrine release of a number of peptide hormones, including cholecystokinin (CCK) and 5-hydroxytryptamine (5-HT). Systemic administration of CCK octapeptide inhibits a subset of presympathetic neurons of the rostroventrolateral medulla (RVLM) that may be responsible for driving the sympathetic vasomotor tone to the GI viscera. The aim of this study was to determine whether endogenous release of CCK and/or 5-HT also inhibits CCK-sensitive RVLM neurons. The effects of intraduodenal administration of the secretagogues sodium oleate (SO) and soybean trypsin inhibitor (SBTI) on circulating levels of CCK and 5-HT were examined. In separate experiments, the discharge rates of barosensitive, medullospinal, CCK-sensitive RVLM presympathetic vasomotor neurons were recorded after rapid intraduodenal infusion of SO-SBTI or water. Alternatively, animals were pretreated with the CCK1 receptor antagonists devazepide and lorglumide or the 5-HT3 antagonist MDL-72222 before SO-SBTI administration. Secretagogue infusion significantly increased the level of circulating CCK, but not 5-HT. SO-SBTI significantly decreased (58%) the neuronal firing rate of CCK-sensitive RVLM neurons compared with water (5%). CCK1 receptor antagonists did not reverse SO-SBTI-induced neuronal inhibition (58%), whereas the 5-HT3 antagonist significantly attenuated the effect (22%). This study demonstrates a functional relation between a subset of RVLM presympathetic vasomotor neurons and meal-related signals arising from the GI tract. It is likely that endogenously released 5-HT acts in a paracrine fashion on GI 5-HT3 receptors to initiate reflex inhibition of these neurons, resulting in GI vasodilatation by withdrawal of sympathetic tone.
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Canabal, Debra D., Zhentao Song, Joseph G. Potian, Annie Beuve, Joseph J. McArdle, and Vanessa H. Routh. "Glucose, insulin, and leptin signaling pathways modulate nitric oxide synthesis in glucose-inhibited neurons in the ventromedial hypothalamus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 4 (April 2007): R1418—R1428. http://dx.doi.org/10.1152/ajpregu.00216.2006.
Full textAbstract:
Glucose-sensing neurons in the ventromedial hypothalamus (VMH) are involved in the regulation of glucose homeostasis. Glucose-sensing neurons alter their action potential frequency in response to physiological changes in extracellular glucose, insulin, and leptin. Glucose-excited neurons decrease, whereas glucose-inhibited (GI) neurons increase, their action potential frequency when extracellular glucose is reduced. Central nitric oxide (NO) synthesis is regulated by changes in local fuel availability, as well as insulin and leptin. NO is involved in the regulation of food intake and is altered in obesity and diabetes. Thus this study tests the hypothesis that NO synthesis is a site of convergence for glucose, leptin, and insulin signaling in VMH glucose-sensing neurons. With the use of the NO-sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein in conjunction with the membrane potential-sensitive dye fluorometric imaging plate reader, we found that glucose and leptin suppress, whereas insulin stimulates neuronal nitric oxide synthase (nNOS)-dependent NO production in cultured VMH GI neurons. The effects of glucose and leptin were mediated by suppression of AMP-activated protein kinase (AMPK). The AMPK activator 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside (AICAR) increased both NO production and neuronal activity in GI neurons. In contrast, the effects of insulin on NO production were blocked by the phosphoinositide 3-kinase inhibitors wortmannin and LY-294002. Furthermore, decreased glucose, insulin, and AICAR increase the phosphorylation of VMH nNOS, whereas leptin decreases it. Finally, VMH neurons express soluble guanylyl cyclase, a downstream mediator of NO signaling. Thus NO may mediate, in part, glucose, leptin, and insulin signaling in VMH glucose-sensing neurons.
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Wechselberger, Martin, Chadwick L. Wright, Georgia A. Bishop, and Jack A. Boulant. "Ionic channels and conductance-based models for hypothalamic neuronal thermosensitivity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 3 (September 2006): R518—R529. http://dx.doi.org/10.1152/ajpregu.00039.2006.
Full textAbstract:
Thermoregulatory responses are partially controlled by the preoptic area and anterior hypothalamus (PO/AH), which contains a mixed population of temperature-sensitive and insensitive neurons. Immunohistochemical procedures identified the extent of various ionic channels in rat PO/AH neurons. These included pacemaker current channels [i.e., hyperpolarization-activated cyclic nucleotide-gated channels (HCN)], background potassium leak channels (TASK-1 and TRAAK), and transient receptor potential channel (TRP) TRPV4. PO/AH neurons showed dense TASK-1 and HCN-2 immunoreactivity and moderate TRAAK and HCN-4 immunoreactivity. In contrast, the neuronal cell bodies did not label for TRPV4, but instead, punctate labeling was observed in traversing axons or their terminal endings. On the basis of these results and previous electrophysiological studies, Hodgkin–Huxley-like models were constructed. These models suggest that most PO/AH neurons have the same types of ionic channels, but different levels of channel expression can explain the inherent properties of the various types of temperature-sensitive and insensitive neurons.
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Peters, J. H., R. C. Ritter, and S. M. Simasko. "Leptin and CCK selectively activate vagal afferent neurons innervating the stomach and duodenum." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 6 (June 2006): R1544—R1549. http://dx.doi.org/10.1152/ajpregu.00811.2005.
Full textAbstract:
The hormone leptin and the gut peptide CCK synergistically interact to enhance the process of satiation. Although this interaction may occur at several levels of the neuroaxis, our previous results indicate that leptin can specifically enhance the satiation effect of CCK by acting on subdiaphragmatic vagal afferent neurons. Because of this localized action, we hypothesized that a high proportion of vagal afferent neurons innervating the stomach or duodenum would be responsive to leptin and/or CCK. To test this hypothesis, we measured changes in cytosolic calcium levels induced by leptin and CCK in cultured nodose ganglion neurons labeled with a retrograde neuronal tracer injected into either the stomach or the duodenum. In the neurons labeled from the stomach, CCK activated 74% (39 of 53) compared with only 35% (34 of 97) of nonlableled cells. Of the CCK-responsive neurons 60% (18 of 30) were capsaicin-sensitive. Leptin activated 42% (22 of 53) of the stomach innervating neurons compared with 26% of nonlabeled neurons. All of the leptin-sensitive neurons labeled from the stomach also responded to CCK. In the neurons labeled from the duodenum, CCK activated 71% (20 of 28). Of these CCK-responsive neurons 80% (12 of 15) were capsaicin sensitive. Leptin activated 46% (13 of 28) of these duodenal innervating neurons, of which 89% (8 of 9) were capsaicin-sensitive. Among neurons labeled from the duodenum 43% (12 of 28) were responsive to both leptin and CCK, compared with only 15% (15 of 97) of unlabeled neurons. Our results support the hypothesis that vagal afferent sensitivity to CCK and leptin is concentrated in neurons that innervate the stomach and duodenum. These specific visceral afferent populations are likely to comprise a substrate through which acute leptin/CCK interactions enhance satiation.
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Medan, Violeta, Damián Oliva, and Daniel Tomsic. "Characterization of Lobula Giant Neurons Responsive to Visual Stimuli That Elicit Escape Behaviors in the Crab Chasmagnathus." Journal of Neurophysiology 98, no. 4 (October 2007): 2414–28. http://dx.doi.org/10.1152/jn.00803.2007.
Full textAbstract:
In the grapsid crab Chasmagnathus, a visual danger stimulus elicits a strong escape response that diminishes rapidly on stimulus repetition. This behavioral modification can persist for several days as a result of the formation of an associative memory. We have previously shown that a generic group of large motion-sensitive neurons from the lobula of the crab respond to visual stimuli and accurately reflect the escape performance. Additional evidence indicates that these neurons play a key role in visual memory and in the decision to initiate an escape. Although early studies recognized that the group of lobula giant (LG) neurons consisted of different classes of motion-sensitive cells, a distinction between these classes has been lacking. Here, we recorded in vivo the responses of individual LG neurons to a wide range of visual stimuli presented in different segments of the animal's visual field. Physiological characterizations were followed by intracellular dye injections, which permitted comparison of the functional and morphological features of each cell. All LG neurons consisted of large tangential arborizations in the lobula with axons projecting toward the midbrain. Functionally, these cells proved to be more sensitive to single objects than to flow field motion. Despite these commonalities, clear differences in morphology and physiology allowed us to identify four distinct classes of LG neurons. These results will permit analysis of the role of each neuronal type for visually guided behaviors and will allow us to address specific questions on the neuronal plasticity of LGs that underlie the well-recognized memory model of the crab.
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Cummins, T. R., Y. Xia, and G. G. Haddad. "Functional properties of rat and human neocortical voltage-sensitive sodium currents." Journal of Neurophysiology 71, no. 3 (March 1, 1994): 1052–64. http://dx.doi.org/10.1152/jn.1994.71.3.1052.
Full textAbstract:
1. The functional properties of sodium currents in acutely dissociated adult human, neonatal rat [postnatal day (P) 3 and P10], and mature rat (P21-23) neocortical pyramidal neurons were studied using whole-cell patch-clamp techniques. 2. The voltage dependence of activation and steady-state inactivation of neonatal rat sodium currents was shifted in the positive direction when compared with mature rat sodium currents. In contrast, no difference was detected between the voltage dependence of activation and steady-state inactivation of mature rat and adult human sodium currents. 3. The fast inactivation of rat (neonatal and mature) and human neocortical sodium currents were best fit with three components; a fast decay component, a slow decay component, and a persistent component. The magnitude of the persistent current in neocortical neurons averaged 1-3% of the peak current. Inactivation was faster for sodium currents in neonatal rat neocortical neurons than in mature neurons. No difference was detected in the kinetics of inactivation between mature rat and adult human sodium currents. 4. Saxitoxin (STX) inhibited neuronal sodium currents at nanomolar concentrations in neonatal and mature rat and adult human neocortical neurons. STX-insensitive channels were not detected. 5. STX affinity was also assayed using 3H-STX. A single high-affinity binding site was found in neonatal rat, mature rat, and adult human neocortical tissue. A developmental increase in STX binding site density in the rat neocortex was tightly correlated with the increase in the sodium current density (normalized to cell capacitance). Human neocortical tissue and mature rat neocortical tissue did not differ in STX binding site density or sodium current density. 6. From these electrophysiological and autoradiographic studies we conclude that 1) the increase in the normalized sodium current density and STX binding density with age postnatally reflects an increase in binding sites of sodium channels functionally expressed on neuronal membranes, 2) the functional differences in channel behavior with maturation can explain the higher threshold for excitation in neonatal neocortical neurons and the increase in accommodation or adaptation in firing in the mature neuron, and 3) mature rat neocortical neurons represent a valid model for the study of adult human pyramidal neocortical neurons in terms of Na+ channel expression and function.
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Verberne, Anthony J. M., and Daniela M. Sartor. "CCK-induced inhibition of presympathetic vasomotor neurons: dependence on subdiaphragmatic vagal afferents and central NMDA receptors in the rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 4 (October 2004): R809—R816. http://dx.doi.org/10.1152/ajpregu.00258.2004.
Full textAbstract:
Systemic administration of cholecystokinin (CCK) inhibits a subpopulation of rostral ventrolateral medulla (RVLM) presympathetic vasomotor neurons. This study was designed to determine whether this effect involved subdiaphragmatic vagal afferents and/or central N-methyl-d-aspartic acid (NMDA) receptors. Recordings were made from CCK-sensitive RVLM presympathetic vasomotor neurons in halothane-anesthetized, paralyzed male Sprague-Dawley rats. The responses of the neurons to CCK (2 and 4 μg/kg iv), phenylephrine (PE; 5 μg/kg iv), and phenylbiguanide (PBG; 5 μg/kg iv) were tested before and after application of the local anesthetic lidocaine (2% wt/vol gel; 1 ml) to the subdiaphragmatic vagi at the level of the esophagus. In seven separate experiments, lidocaine markedly reduced the inhibitory effects of CCK on RVLM presympathetic neuronal discharge rate. In other experiments, the effect of systemic administration of dizocilpine (1 mg/kg iv), a noncompetitive antagonist at NMDA receptor ion channels, on the RVLM presympathetic neuronal responses to CCK, PBG, and PE was tested. In all cases ( n = 6 neurons in 6 individual rats), dizocilpine inhibited the effects of CCK, PBG, and PE on RVLM presympathetic neuronal discharge. These results suggest that the effects of systemic CCK on the discharge of RVLM presympathetic neurons is mediated via an action on receptors located on subdiaphragmatic vagal afferents. Furthermore, the data suggest that CCK activates a central pathway involving NMDA receptors to produce inhibition of RVLM presympathetic neuronal discharge.
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Fu, Xin, Huan Ye, Huijuan Jia, Xin Wang, Taylor Chomiak, and Feng Luo. "Muscarinic acetylcholine receptor-dependent persistent activity of layer 5 intrinsic-bursting and regular-spiking neurons in primary auditory cortex." Journal of Neurophysiology 122, no. 6 (December 1, 2019): 2344–53. http://dx.doi.org/10.1152/jn.00184.2019.
Full textAbstract:
Cholinergic signaling coupled to sensory-driven neuronal depolarization is essential for modulating lasting changes in deep-layer neural excitability and experience-dependent plasticity in the primary auditory cortex. However, the underlying cellular mechanism(s) associated with coincident cholinergic receptor activation and neuronal depolarization of deep-layer cortical neurons remains unknown. Using in vitro whole cell patch-clamp recordings targeted to neurons ( n = 151) in isolated brain slices containing the primary auditory cortex (AI), we investigated the effects of cholinergic receptor activation and neuronal depolarization on the electrophysiological properties of AI layer 5 intrinsic-bursting and regular-spiking neurons. Bath application of carbachol (5 µM; cholinergic receptor agonist) paired with suprathreshold intracellular depolarization led to persistent activity in these neurons. Persistent activity may involve similar cellular mechanisms and be generated intrinsically in both intrinsic-bursting and regular-spiking neurons given that it 1) persisted under the blockade of ionotropic glutamatergic (kynurenic acid, 2 mM) and GABAergic receptors (picrotoxin, 100 µM), 2) was fully blocked by both atropine (10 µM; nonselective muscarinic antagonist) and flufenamic acid [100 µM; nonspecific Ca2+-sensitive cationic channel (CAN) blocker], and 3) was sensitive to the voltage-gated Ca2+ channel blocker nifedipine (50 µM) and Ca2+-free artificial cerebrospinal fluid. Together, our results support a model through which coincident activation of AI layer 5 neuron muscarinic receptors and suprathreshold activation can lead to sustained changes in layer 5 excitability, providing new insight into the possible role of a calcium-CAN-dependent cholinergic mechanism of AI cortical plasticity. These findings also indicate that distinct streams of auditory processing in layer 5 intrinsic-bursting and regular-spiking neurons may run in parallel during learning-induced auditory plasticity. NEW & NOTEWORTHY Cholinergic signaling coupled to sensory-driven neuronal depolarization is essential for modulating lasting changes in experience-dependent plasticity in the primary auditory cortex. Cholinergic activation together with cellular depolarization can lead to persistent activity in both intrinsic-bursting and regular-spiking layer 5 pyramidal neurons. A similar mechanism involving muscarinic acetylcholine receptor, voltage-gated Ca2+ channel, and possible Ca2+-sensitive nonspecific cationic channel activation provides new insight into our understanding of the cellular mechanisms that govern learning-induced auditory cortical and subcortical plasticity.
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Chiquet, M., and J. G. Nicholls. "Neurite outgrowth and synapse formation by identified leech neurones in culture." Journal of Experimental Biology 132, no. 1 (September 1, 1987): 191–206. http://dx.doi.org/10.1242/jeb.132.1.191.
Full textAbstract:
After injury, neurones in the central nervous system (CNS) of the leech regenerate with a high degree of specificity. The aim of our experiments has been to study the sequential steps involved in neurite growth and synapse formation using isolated identified neurones in culture. An important requirement for sprouting of leech neurones is the substrate. Neurites grow only slowly and sparsely on polylysine or vertebrate laminin. The extracellular matrix of leech ganglion capsules contains a protease-sensitive factor which can be extracted with urea. With this material as substrate, growth proceeds rapidly in defined medium. Another neurite-promoting substrate is provided by the plant lectin concanavalin A (Con A). The activity of Con A, but not of the capsule matrix factor, is blocked by the Con A-specific hapten methyl alpha-D-mannoside. The morphology and branching pattern of the neurites in culture depend on the specific substrate and on the type of neurone. During stimulation, less Ca2+ uptake occurs into growth cones than in cell bodies. The mechanism of neurite growth seems not to depend on activity-mediated Ca2+ influx or on interactions between neuronal cell surfaces. However, even without profuse outgrowth, electrical and chemical synapses develop between neighbouring neurones. The type of synapse depends predictably on the types of neurones within the cell pair. Since the development of a synapse can be followed with time in culture, the sequential events can each be studied separately for this multi-step process.
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Irani, Boman G., Christelle Le Foll, Ambrose A. Dunn-Meynell, and Barry E. Levin. "Ventromedial nucleus neurons are less sensitive to leptin excitation in rats bred to develop diet-induced obesity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 3 (March 2009): R521—R527. http://dx.doi.org/10.1152/ajpregu.90842.2008.
Full textAbstract:
Maternal obesity accentuates offspring obesity in dams bred to develop diet-induced obesity (DIO) on a 31% fat, high energy (HE) diet but has no effect on offspring of diet-resistant (DR) dams. Only DIO dams became obese on HE diet when they and DR dams were fed 5% fat chow or HE diets throughout gestation and lactation. Leptin sensitivity of dissociated arcuate (ARC) and ventromedial (VMN) hypothalamic nucleus neurons from the 3- to 4-wk-old offspring was assessed using fura-2 calcium imaging to monitor leptin-induced changes in intracellular calcium ([Ca2+]i) as an index of neuronal activity. At 0.1, 1, 10 fmol/l leptin, ∼4 times more VMN and ARC neurons were excited than inhibited by leptin. In the VMN, leptin excited up to 41% fewer neurons, and these excited neurons were less sensitive to increasing doses of leptin in DIO compared with DR offspring. Also, maternal HE diet intake decreased the percentage of leptin-excited VMN neurons in both DIO and DR offspring and decreased the percentage of leptin-inhibited VMN neurons by 36% only in DIO offspring. In the ARC, there were no genotype or maternal diet effects on the percentage of ARC neurons excited by leptin. However, those DR neurons that were leptin excited were more sensitive to leptin than were those from DIO offspring. These data suggest that reduced responsiveness of DIO VMN neurons to leptin's excitatory effects may be an important contributing factor to the reduced anorectic and thermogenic leptin responsiveness of DIO rats in vivo.
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Xue, Jin, Dan Zhou, Hang Yao, and Gabriel G. Haddad. "Role of transporters and ion channels in neuronal injury under hypoxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 2 (February 2008): R451—R457. http://dx.doi.org/10.1152/ajpregu.00528.2007.
Full textAbstract:
The aims of the current study were to 1) examine the effects of hypoxia and acidosis on cultured cortical neurons and 2) explore the role of transporters and ion channels in hypoxic injury. Cell injury was measured in cultured neurons or hippocampal slices following hypoxia (1% O2) or acidosis (medium pH 6.8) treatment. Inhibitors of transporters and ion channels were employed to investigate their roles in hypoxic injury. Our results showed that 1) neuronal damage was apparent at 5–7 days of hypoxia exposure, i.e., 36–41% of total lactate dehydrogenase was released to medium and 2) acidosis alone did not lead to significant injury compared with nonacidic, normoxic controls. Pharmacological studies revealed 1) no significant difference in neuronal injury between controls (no inhibitor) and inhibition of Na+-K+-ATP pump, voltage-gated Na+ channel, ATP-sensitive K+ channel, or reverse mode of Na+/Ca2+ exchanger under hypoxia; however, 2) inhibition of NBCs with 500 μM DIDS did not cause hypoxic death in either cultured cortical neurons or hippocampal slices; 3) in contrast, inhibition of Na+/H+ exchanger isoform 1 (NHE1) with either 10 μM HOE-642 or 2 μM T-162559 resulted in dramatic hypoxic injury (+95% for HOE-642 and +100% for T-162559 relative to normoxic control, P < 0.001) on treatment day 3, when no death occurred for hypoxic controls (no inhibitor). No further damage was observed by NHE1 inhibition on treatment day 5. We conclude that inhibition of NHE1 accelerates hypoxia-induced neuronal damage. In contrast, DIDS rescues neuronal death under hypoxia. Hence, DIDS-sensitive mechanism may be a potential therapeutic target.
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Burbaud, P., C. Doegle, C. Gross, and B. Bioulac. "A quantitative study of neuronal discharge in areas 5, 2, and 4 of the monkey during fast arm movements." Journal of Neurophysiology 66, no. 2 (August 1, 1991): 429–43. http://dx.doi.org/10.1152/jn.1991.66.2.429.
Full textAbstract:
1. The properties of parietal neurons were studied in four adult rhesus monkeys during fast arm movements. The animals were trained to perform flexion or extension of the forearm about the elbow in response to specific auditory cues. Single neuron activity was recorded in 272 area 5 neurons, 81 neurons of the somatosensory cortex, and 92 neurons of the motor cortex. 2. In area 5, 42% of neuronal changes occurred before movement onset (early changes) and 58% after (late changes), with 21% before the earliest electromyogram. The range of modification in activity took place between 260 ms before movement onset and 180 ms after. Complex receptive fields were found in area 5 with a greater proportion among the late neurons (72%) than among the early neurons (32%). 3. Different patterns of activity were observed in neurons recorded in both movement directions. Reciprocal neurons represented 52% of the motor cortex neurons and 41% of the neurons in the somatosensory cortex but only 14% of the area 5 neurons. Of the remainder area 5 neurons, 46% were direction-sensitive neurons and 39% coactivated neurons. This suggests a more complex encoding of movement direction in area 5 than in area 2 or 4. 4. Temporal characteristics of the neuronal bursts were quantitatively analyzed in areas 5, 2, and 4. Neuronal burst duration was longer in area 5 than in the other areas. Above all, a variability of burst parameters, which did not depend on variable movement execution, was noticed in area 5. Therefore neuronal activity in this cortical area cannot be simply explained by a convergence of sensory and motor inputs but may depend on the behavioral context in which the movement is performed. 5. A correlation between neuronal burst duration and movement duration was found in 41% of area 2 neurons. In area 5, this correlation was observed in 20% of the late neurons and in 14% of the early neurons. A correlation between neuronal discharge frequency and movement velocity was found in 34% of area 2 neurons and 24% of area 4 neurons. About 16% of both late and early neurons in area 5 showed such a correlation. These neurons received polyarticular input, and it is suggested that they may be involved in the kinematic encoding of polyarticular movements. 6. A topographic and functional organization of area 5 was noticed. In anterior area, 5, 83% of the neurons had receptive fields and most of the reciprocal neurons and those exhibiting a correlation with movement parameters were found there.(ABSTRACT TRUNCATED AT 400 WORDS)
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Bonnot, Agnès, George Z. Mentis, Jesse Skoch, and Michael J. O'Donovan. "Electroporation Loading of Calcium-Sensitive Dyes Into the CNS." Journal of Neurophysiology 93, no. 3 (March 2005): 1793–808. http://dx.doi.org/10.1152/jn.00923.2004.
Full textAbstract:
Calcium imaging of neural network function has been limited by the extent of tissue labeled or the time taken for labeling. We now describe the use of electroporation—an established technique for transfecting cells with genes—to load neurons with calcium-sensitive dyes in the isolated spinal cord of the neonatal mouse in vitro. The dyes were injected subdurally, intravascularly, or into the central canal. This technique results in rapid and extensive labeling of neurons and their processes at all depths of the spinal cord, over a rostrocaudal extent determined by the position and size of the electrodes. Our results suggest that vascular distribution of the dye is involved in all three types of injections. Electroporation disrupts local reflex and network function only transiently (∼1 h), after which time they recover. We describe applications of the method to image activity of neuronal populations and individual neurons during antidromic, reflex, and locomotor-like behaviors. We show that these different motor behaviors are characterized by distinct patterns of activation among the labeled populations of cells.
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Leathers, Marvin L., and Carl R. Olson. "In monkeys making value-based decisions, amygdala neurons are sensitive to cue value as distinct from cue salience." Journal of Neurophysiology 117, no. 4 (April 1, 2017): 1499–511. http://dx.doi.org/10.1152/jn.00564.2016.
Full textAbstract:
Neurons in the lateral intraparietal (LIP) area of macaque monkey parietal cortex respond to cues predicting rewards and penalties of variable size in a manner that depends on the motivational salience of the predicted outcome (strong for both large reward and large penalty) rather than on its value (positive for large reward and negative for large penalty). This finding suggests that LIP mediates the capture of attention by salient events and does not encode value in the service of value-based decision making. It leaves open the question whether neurons elsewhere in the brain encode value in the identical task. To resolve this issue, we recorded neuronal activity in the amygdala in the context of the task employed in the LIP study. We found that responses to reward-predicting cues were similar between areas, with the majority of reward-sensitive neurons responding more strongly to cues that predicted large reward than to those that predicted small reward. Responses to penalty-predicting cues were, however, markedly different. In the amygdala, unlike LIP, few neurons were sensitive to penalty size, few penalty-sensitive neurons favored large over small penalty, and the dependence of firing rate on penalty size was negatively correlated with its dependence on reward size. These results indicate that amygdala neurons encoded cue value under circumstances in which LIP neurons exhibited sensitivity to motivational salience. However, the representation of negative value, as reflected in sensitivity to penalty size, was weaker than the representation of positive value, as reflected in sensitivity to reward size. NEW & NOTEWORTHY This is the first study to characterize amygdala neuronal responses to cues predicting rewards and penalties of variable size in monkeys making value-based choices. Manipulating reward and penalty size allowed distinguishing activity dependent on motivational salience from activity dependent on value. This approach revealed in a previous study that neurons of the lateral intraparietal (LIP) area encode motivational salience. Here, it reveals that amygdala neurons encode value. The results establish a sharp functional distinction between the two areas.
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Deitmer, Joachim W., Roger Eckert, and Wolf-R. Schlue. "Changes in the intracellular free calcium concentration of Aplysia and leech neurones measured with calcium-sensitive microelectrodes." Canadian Journal of Physiology and Pharmacology 65, no. 5 (May 1, 1987): 934–39. http://dx.doi.org/10.1139/y87-149.
Full textAbstract:
The intracellular free Ca concentration was measured in invertebrate neurones using single-barrelled and double-barrelled neutral-carrier microelectrodes. The electrodes were calibrated in solutions containing different Ca concentrations between 1 mM and 0.01 μM. The electrode responses were also tested at different ionic strengths and at varying Na concentrations. The electrodes responded with 25–30 mV per 10-fold change in Ca concentration between 1 mM and 1 μM and with 10–25 mV between 1 and 0.1 μM Ca. The intracellular free Ca concentration was measured to be between 0.1 and 0.7 μM in the neurones. The changes of intracellular Ca in identified voltage-clamped neurones of Aplysia californica were recorded during iontophoretic injections of Ca2+ or EGTA. The decrease of intracellular Ca following EGTA injection was correlated with the suppression of the Ca-dependent K current and with the reduction of Ca-induced inactivation of voltage-dependent Ca current. In identified neurones of the leech Hirudo medicinalis a reversible increase of intracellular Ca2+ was recorded after inhibition of the Na–K pump, either by addition of ouabain (0.5 mM) or by lowering the external K concentration (0.2 mM). This rise in intracellular Ca2+ did not occur, and was even reversed, in the absence of external Na, suggesting the existence of Na–Ca exchange across the leech neuronal membrane.
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Nadeau, H., and H. A. Lester. "NRSF Causes cAMP-Sensitive Suppression of Sodium Current in Cultured Hippocampal Neurons." Journal of Neurophysiology 88, no. 1 (July 1, 2002): 409–21. http://dx.doi.org/10.1152/jn.2002.88.1.409.
Full textAbstract:
The neuron restrictive silencer factor (NRSF/REST) has been shown to bind to the promoters of many neuron-specific genes and is able to suppress transcription of Na+channels in PC12 cells, although its functional effect in terminally differentiated neurons is unknown. We constructed lentiviral vectors to express NRSF as a bicistronic message with green fluorescent protein (GFP) and followed infected hippocampal neurons in culture over a period of 1–2 wk. NRSF-expressing neurons showed a time-dependent suppression of Na+channel function as measured by whole cell electrophysiology. Suppression was reversed or prevented by the addition of membrane-permeable cAMP analogues and enhanced by cAMP antagonists but not affected by increasing protein expression with a viral enhancer. Secondary effects, including altered sensitivity to glutamate and GABA and reduced outward K+currents, were duplicated by culturing GFP-infected control neurons in TTX. The striking similarity of the phenotypes makes NRSF potentially useful as a genetic “silencer” and also suggests avenues of further exploration that may elucidate the transcription factor's in vivo role in neuronal plasticity.
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Albeck, Y., and M. Konishi. "Responses of neurons in the auditory pathway of the barn owl to partially correlated binaural signals." Journal of Neurophysiology 74, no. 4 (October 1, 1995): 1689–700. http://dx.doi.org/10.1152/jn.1995.74.4.1689.
Full textAbstract:
1. Extracellular single-unit recording in anesthetized barn owls was used to study neuronal response to dichotic stimuli of variable binaural correlation (BC). Recordings were made in the output fibers of nucleus laminaris (NL), the anterior division of the ventral lateral lemniscal nucleus (VLVa), the core of the central nucleus of the inferior colliculus (ICcC), the lateral shell of the central nucleus of the inferior colliculus (ICcLS), and the external nucleus of the inferior colliculus (ICx). 2. The response of all neurons sensitive to interaural time difference (ITD) varied with BC. The relationship between BC and impulse number fits a linear, a parabolic, or a ramp model. A linear or parabolic model fits most neurons in low-level nuclei. Higher order neurons in ICx did not respond to noise bursts with strong negative binaural correlation, creating a ramp-like response to BC. 3. A neuron's ability to detect ITD varied as a function of BC. Conversely, a neuron's response to BC changed with ITD. Neurons in NL, VLVa, and ICcC show almost periodic ITD response curves. In these neurons peaks and troughs of ITD response curves diminished as BC decreased, creating a flat ITD response when BC = 0. When BC was set to -1, the most favorable ITD became the least favorable one and vice versa. The ITD response curve of ICx neurons usually has a single dominant peak. The response of those neurons to a negatively correlated noise pair (BC = -1) showed two ITD peaks, flanking the position of the primary peak. 4. The parabolic BC response of NL neurons fits the prediction of the cross-correlation model, assuming half-wave rectification of the sound by the cochlea. Linear response is not predicted by the model. However, the parabolic and the linear neurons probably do not belong to two distinct groups as the difference between them is not statistically significant. Thus, the cross-correlation model provides a good description of the binaural response not only in NL but also in VLVa and ICcC. 5. Almost all ramp neurons occurred in either ICx or ICcLS where neurons are more broadly tuned to frequency than those in the lower nuclei. The synthesis of this response type requires, however, not only the convergence of different frequency channels but also inhibition between different ITD channels. We modeled the ramp response as a three-step process. First, different spectral channels converge to create broad frequency tuning. The response to variation in BC will be linear (or parabolic) because it is a sum of linear (parabolic) responses. Second, the activity in some adjacent ITD channels is subtracted by lateral inhibition. Finally, the result is rectified using a high threshold to avoid negative activity.
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Riediger, Thomas, Nicole Eisele, Caroline Scheel, and Thomas A. Lutz. "Effects of glucagon-like peptide 1 and oxyntomodulin on neuronal activity of ghrelin-sensitive neurons in the hypothalamic arcuate nucleus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 4 (April 2010): R1061—R1067. http://dx.doi.org/10.1152/ajpregu.00438.2009.
Full textAbstract:
Glucagon-like peptide 1 (GLP-1) and oxyntomodulin (OXM) are structurally related gastrointestinal hormones that are secreted in response to food intake. They reduce food intake and body weight and exert partly overlapping actions on glucose homeostasis and gastrointestinal function. The hypothalamic arcuate (ARC) nucleus is among the central structures expressing a high density of GLP-1 receptors (GLP-1R), which are known to be activated by both peptides. It was the aim of our electrophysiological studies to characterize the effects of GLP-1 and OXM on functionally defined ghrelin-sensitive ARC neurons. GLP-1 and OXM (10−7 M) exerted excitatory effects in about two-thirds of ghrelin-inhibited neurons and in approximately one-third of ghrelin-excited cells. In addition, a minor fraction of the ghrelin-excited cells was inhibited by both peptides. There was a high degree of cosensitivity to GLP-1 and OXM, and the effects of both hormones were blocked by the GLP-1R antagonist exendin(9–39). The GLP-1R-mediated excitations and inhibitions persisted under synaptic blockade, indicating a direct postsynaptic mode of action. Our results demonstrate that GLP-1 and OXM directly and similarly alter neuronal activity in the ARC, probably via a common GLP-1R-mediated mechanism. Ghrelin-antagonistic effects on neuronal activity, which might be implicated in ghrelin-antagonistic in vivo actions, resulting from GLP-1R stimulation (e.g., GLP-1R dependent supression of food intake), predominated in ghrelin-inhibited ARC neurons. However, a subset of ghrelin-excited ARC neurons showed responses to OXM or GLP-1, suggesting the existence of a common mode of action for these hormones; the functional relevance of this effect remains to be elucidated.
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Soffe, S. R., and K. T. Sillar. "Patterns of synaptic drive to ventrally located spinal neurones in Rana temporaria embryos during rhythmic and non-rhythmic motor responses." Journal of Experimental Biology 156, no. 1 (March 1, 1991): 101–18. http://dx.doi.org/10.1242/jeb.156.1.101.
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1. Intracellular recordings have been made from ventrally located neurones in the spinal cord of Rana temporaria embryos at around the time of hatching. Both short-latency ‘reflex’ and more prolonged rhythmic motor responses can be elicited by stimulation of the skin in immobilized embryos. Initial responses to single-sided skin stimuli usually involve excitation of neurones on the opposite side and strychnine-sensitive inhibition of neurones on the same side. Less reliable responses to dimming the lights also involve initial excitation on one side associated with inhibition on the opposite side. 2. Intracellular recordings from single neurones during rhythmic activity show that on each cycle the same neurone can fire one or many spikes during the course of a single evoked or spontaneous episode. Bursts occur at longer cycle periods, generally at the start of episodes; single spikes occur at shorter cycle periods, generally later in episodes. 3. During sustained rhythmic responses, neuronal membrane potential is generally depolarised and returns gradually to its resting level at the end of the episode. During the episode, relatively depolarising phases of synaptic excitation alternate with relatively hyperpolarising phases of chloride-dependent synaptic inhibition. Cell input resistance is reduced by around 50% throughout each episode. Within each cycle, input resistance is reduced further during the hyperpolarising phase than during the depolarising phase. 4. Rhythmic excitation and inhibition of ventrally located neurones appears to be similar throughout the whole range of cycle periods, supporting the suggestion that a single rhythm-generating system with a wide ‘permissive’ range drives rhythmic movements in R. temporaria embryos.
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Labhart, Thomas, Jürgen Petzold, and Hansruedi Helbling. "Spatial integration in polarization-sensitive interneurones of crickets: a survey of evidence, mechanisms and benefits." Journal of Experimental Biology 204, no. 14 (July 15, 2001): 2423–30. http://dx.doi.org/10.1242/jeb.204.14.2423.
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SUMMARY Many insects exploit the polarization pattern of the sky for compass orientation in navigation or cruising-course control. Polarization-sensitive neurones (POL1-neurones) in the polarization vision pathway of the cricket visual system have wide visual fields of approximately 60° diameter, i.e. these neurones integrate information over a large area of the sky. This results from two different mechanisms. (i) Optical integration; polarization vision is mediated by a group of specialized ommatidia at the dorsal rim of the eye. These ommatidia lack screening pigment, contain a wide rhabdom and have poor lens optics. As a result, the angular sensitivity of the polarization-sensitive photoreceptors is very wide (median approximately 20°). (ii) Neural integration; each POL1-neurone receives input from a large number of dorsal rim photoreceptors with diverging optical axes. Spatial integration in POL1-neurones acts as a spatial low-pass filter. It improves the quality of the celestial polarization signal by filtering out cloud-induced local disturbances in the polarization pattern and increases sensitivity.
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DiCarlo, James J., and John H. R. Maunsell. "Anterior Inferotemporal Neurons of Monkeys Engaged in Object Recognition Can be Highly Sensitive to Object Retinal Position." Journal of Neurophysiology 89, no. 6 (June 2003): 3264–78. http://dx.doi.org/10.1152/jn.00358.2002.
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Visual object recognition is computationally difficult because changes in an object's position, distance, pose, or setting may cause it to produce a different retinal image on each encounter. To robustly recognize objects, the primate brain must have mechanisms to compensate for these variations. Although these mechanisms are poorly understood, it is thought that they elaborate neuronal representations in the inferotemporal cortex that are sensitive to object form but substantially invariant to other image variations. This study examines this hypothesis for image variation resulting from changes in object position. We studied the effect of small differences (±1.5°) in the retinal position of small (0.6° wide) visual forms on both the behavior of monkeys trained to identify those forms and the responses of 146 anterior IT (AIT) neurons collected during that behavior. Behavioral accuracy and speed were largely unaffected by these small changes in position. Consistent with previous studies, many AIT responses were highly selective for the forms. However, AIT responses showed far greater sensitivity to retinal position than predicted from their reported receptive field (RF) sizes. The median AIT neuron showed a ∼60% response decrease between positions within ±1.5° of the center of gaze, and 52% of neurons were unresponsive to one or more of these positions. Consistent with previous studies, each neuron's rank order of target preferences was largely unaffected across position changes. Although we have not yet determined the conditions necessary to observe this marked position sensitivity in AIT responses, we rule out effects of spatial-frequency content, eye movements, and failures to include the RF center. To reconcile this observation with previous studies, we hypothesize that either AIT position sensitivity strongly depends on object size or that position sensitivity is sharpened by extensive visual experience at fixed retinal positions or by the presence of flanking distractors.
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Cottrell, G. A. "The first peptide-gated ion channel." Journal of Experimental Biology 200, no. 18 (September 1, 1997): 2377–86. http://dx.doi.org/10.1242/jeb.200.18.2377.
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Patch-clamp experiments on the C2 neurone of Helix aspersa have shown that the neuropeptide Phe-Met-Arg-Phe-NH2 (FMRFamide) directly gates a Na+ channel. The channel is amiloride-sensitive. Activation of this channel is responsible for the fast excitatory action of the peptide. Using primers based on amiloride-sensitive epithelial Na+ channels, a complete cDNA sequence (FaNaCh) was cloned and sequenced from a Helix library. The sequence is predicted to have just two membrane-spanning regions and a large extracellular loop. When expressed in Xenopus laevis oocytes, the channel responded to FMRFamide. Taken together, these data provide the first evidence for a peptide-gated ion channel. Comparison of the properties of the expressed FaNaCh with the native neuronal channel show small differences in the sensitivities to some drugs and in channel conductance. It is not yet clear whether the native channel is a homo-oligomer or comprises other subunits. The peptide FKRFamide is an effective antagonist of FMRFamide on the expressed and neuronal channels. Nucleotide sequences encoding similar channel proteins occur in neurones of species as dissimilar as man and Caenorhabditis elegans. Some channels are thought to be associated with mechano-sensation, at least one is a proton-gated channel and others may also be ligand-gated channels.
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Hass, Charles A., and Gregory D. Horwitz. "V1 mechanisms underlying chromatic contrast detection." Journal of Neurophysiology 109, no. 10 (May 15, 2013): 2483–94. http://dx.doi.org/10.1152/jn.00671.2012.
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To elucidate the cortical mechanisms of color vision, we recorded from individual primary visual cortex (V1) neurons in macaque monkeys performing a chromatic detection task. Roughly 30% of the neurons that we encountered were unresponsive at the monkeys' psychophysical detection threshold (PT). The other 70% were responsive at threshold but on average, were slightly less sensitive than the monkey. For these neurons, the relationship between neurometric threshold (NT) and PT was consistent across the four isoluminant color directions tested. A corollary of this result is that NTs were roughly four times lower for stimuli that modulated the long- and middle-wavelength sensitive cones out of phase. Nearly one-half of the neurons that responded to chromatic stimuli at the monkeys' detection threshold also responded to high-contrast luminance modulations, suggesting a role for neurons that are jointly tuned to color and luminance in chromatic detection. Analysis of neuronal contrast-response functions and signal-to-noise ratios yielded no evidence for a special set of “cardinal color directions,” for which V1 neurons are particularly sensitive. We conclude that at detection threshold—as shown previously with high-contrast stimuli—V1 neurons are tuned for a diverse set of color directions and do not segregate naturally into red–green and blue–yellow categories.
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Zhang, Hai Xia, and Liu Lin Thio. "Zinc Enhances the Inhibitory Effects of Strychnine-Sensitive Glycine Receptors in Mouse Hippocampal Neurons." Journal of Neurophysiology 98, no. 6 (December 2007): 3666–76. http://dx.doi.org/10.1152/jn.00500.2007.
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Although extracellular Zn2+ is an endogenous biphasic modulator of strychnine-sensitive glycine receptors (GlyRs), the physiological significance of this modulation remains poorly understood. Zn2+ modulation of GlyR may be especially important in the hippocampus where presynaptic Zn2+ is abundant. Using cultured embryonic mouse hippocampal neurons, we examined whether 1 μM Zn2+, a potentiating concentration, enhances the inhibitory effects of GlyRs activated by sustained glycine applications. Sustained 20 μM glycine (EC25) applications alone did not decrease the number of action potentials evoked by depolarizing steps, but they did in 1 μM Zn2+. At least part of this effect resulted from Zn2+ enhancing the GlyR-induced decrease in input resistance. Sustained 20 μM glycine applications alone did not alter neuronal bursting, a form of hyperexcitability induced by omitting extracellular Mg2+. However, sustained 20 μM glycine applications depressed neuronal bursting in 1 μM Zn2+. Zn2+ did not enhance the inhibitory effects of sustained 60 μM glycine (EC70) applications in these paradigms. These results suggest that tonic GlyR activation could decrease neuronal excitability. To test this possibility, we examined the effect of the GlyR antagonist strychnine and the Zn2+ chelator tricine on action potential firing by CA1 pyramidal neurons in mouse hippocampal slices. Co-applying strychnine and tricine slightly but significantly increased the number of action potentials fired during a depolarizing current step and decreased the rheobase for action potential firing. Thus Zn2+ may modulate neuronal excitability normally and in pathological conditions such as seizures by potentiating GlyRs tonically activated by low agonist concentrations.
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Recanzone, Gregg H., Darren C. Guard, Mimi L. Phan, and Tien-I. K. Su. "Correlation Between the Activity of Single Auditory Cortical Neurons and Sound-Localization Behavior in the Macaque Monkey." Journal of Neurophysiology 83, no. 5 (May 1, 2000): 2723–39. http://dx.doi.org/10.1152/jn.2000.83.5.2723.
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Lesion studies have indicated that the auditory cortex is crucial for the perception of acoustic space, yet it remains unclear how these neurons participate in this perception. To investigate this, we studied the responses of single neurons in the primary auditory cortex (AI) and the caudomedial field (CM) of two monkeys while they performed a sound-localization task. Regression analysis indicated that the responses of ∼80% of neurons in both cortical areas were significantly correlated with the azimuth or elevation of the stimulus, or both, which we term “spatially sensitive.” The proportion of spatially sensitive neurons was greater for stimulus azimuth compared with stimulus elevation, and elevation sensitivity was primarily restricted to neurons that were tested using stimuli that the monkeys also could localize in elevation. Most neurons responded best to contralateral speaker locations, but we also encountered neurons that responded best to ipsilateral locations and neurons that had their greatest responses restricted to a circumscribed region within the central 60° of frontal space. Comparing the spatially sensitive neurons with those that were not spatially sensitive indicated that these two populations could not be distinguished based on either the firing rate, the rate/level functions, or on their topographic location within AI. Direct comparisons between the responses of individual neurons and the behaviorally measured sound-localization ability indicated that proportionally more neurons in CM had spatial sensitivity that was consistent with the behavioral performance compared with AI neurons. Pooling the responses across neurons strengthened the relationship between the neuronal and psychophysical data and indicated that the responses pooled across relatively few CM neurons contain enough information to account for sound-localization ability. These data support the hypothesis that auditory space is processed in a serial manner from AI to CM in the primate cerebral cortex.
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Abel, Cornelius, and Manfred Kössl. "Sensitive Response to Low-Frequency Cochlear Distortion Products in the Auditory Midbrain." Journal of Neurophysiology 101, no. 3 (March 2009): 1560–74. http://dx.doi.org/10.1152/jn.90805.2008.
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During auditory stimulation with several frequency components, distortion products (DPs) are generated as byproduct of nonlinear cochlear amplification. After generated, DP energy is reemitted into the ear channel where it can be measured as DP otoacoustic emission (DPOAE), and it also induces an excitatory response at cochlear places related to the DP frequencies. We measured responses of 91 inferior colliculus (IC) neurons in the gerbil during two-tone stimulation with frequencies well above the unit's receptive field but adequate to generate a distinct distortion product (f2-f1 or 2f1-f2) at the unit's characteristic frequency (CF). Neuronal responses to DPs could be accounted for by the simultaneously measured DPOAEs for DP frequencies >1.3 kHz. For DP frequencies <1.3 kHz ( n = 25), there was a discrepancy between intracochlear DP magnitude and DPOAE level, and most neurons responded as if the intracochlear DP level was significantly higher than the DPOAE level in the ear channel. In 12% of those low-frequency neurons, responses to the DPs could be elicited even if the stimulus tone levels were below the threshold level of the neuron at CF. High intracochlear f2-f1 and 2f1-f2 DP-levels were verified by cancellation of the neuronal DP response with a third phase-adjusted tone stimulus at the DP frequency. A frequency-specific reduction of middle ear gain at low frequencies is possibly involved in the reduction of DPOAE level. The results indicate that pitch-related properties of complex stimuli may be produced partially by high intracochlear f2-f1 distortion levels.
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Thompson, Gregory W., Magda Horackova, and J. Andrew Armour. "Ion channel modifying agents influence the electrical activity generated by canine intrinsic cardiac neurons in situ." Canadian Journal of Physiology and Pharmacology 78, no. 4 (March 1, 2000): 293–300. http://dx.doi.org/10.1139/y99-138.
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This study was designed to establish whether agents known to modify neuronal ion channels influence the behavior of mammalian intrinsic cardiac neurons in situ and, if so, in a manner consistent with that found previously in vitro. The activity generated by right atrial neurons was recorded extracellularly in varying numbers of anesthetized dogs before and during continuous local arterial infusion of several neuronal ion channel modifying agents. Veratridine (7.5 µM), the specific modifier of Na+-selective channels, increased neuronal activity (95% above control) in 80% of dogs tested (n = 25). The membrane depolarizing agent potassium chloride (40 mM) reduced neuronal activity (43% below control) in 84% of dogs tested (n = 19). The inhibitor of voltage-sensitive K+ channels, tetraethylammonium (10 mM), decreased neuronal activity (42% below control) in 73% of dogs tested (n = 11). The nonspecific potassium channel inhibitor barium chloride (5 mM) excited neurons (47% above control) in 13 of 19 animals tested. Cadmium chloride (200 µM), which inhibits Ca2+-selective channels and Ca2+-dependent K+ channels, increased neuronal activity (65% above control) in 79% of dogs tested (n = 14). The specific L-type Ca2+ channel blocking agent nifedipine (5 µM) reduced neuronal activity (52% blow control in 72% of 11 dogs tested), as did the nonspecific inhibitor of L-type Ca2+ channels, nickel chloride (5 mM) (36% below control in 69% of 13 dogs tested). Each agent induced either excitatory or inhibitory responses, depending on the agent tested. It is concluded that specific ion channels (INa, ICaL, IKv, and IKCa) that have been associated with intrinsic cardiac neurons in vitro are involved in their capacity to generate action potentials in situ.Key words: calcium channels, intrinsic cardiac neuron, potassium channels, sodium channels.
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Sikdar, S. K., and Y. Oomura. "Selective inhibition of glucose-sensitive neurons in rat lateral hypothalamus by noxious stimuli and morphine." Journal of Neurophysiology 53, no. 1 (January 1, 1985): 17–31. http://dx.doi.org/10.1152/jn.1985.53.1.17.
Full textAbstract:
On the basis of their responsiveness to electrophoretically applied glucose, neurons in the lateral hypothalamic area (LHA) have been characterized as either glucose sensitive or glucose nonsensitive. Glucose-sensitive neurons are important in feeding control (4, 36-38, 44, 54). The aim of this study was to increase understanding of the neurophysiological mechanisms involved in the disturbance of feeding by pain. Radiant heating of the scrotum, strong tail pinch, and immersion of the tail in hot water were used as noxious stimuli. In order to correlate the responses of LHA neurons to noxious inputs with possible local release of endogenous opiates, effects of electrophoretically applied morphine and naloxone were also tested. The effects of glucose, morphine, and noxious stimulation were studied in a total of 165 neurons recorded from 75 adult male urethane-chloralose-anesthetized rats. Of 52 neurons determined to be glucose sensitive, 36 (69%) were inhibited by both noxious stimulation and morphine. A majority of the glucose-nonsensitive neurons did not respond to either morphine or noxious stimulation (87/113, 74%). The relation of glucose sensitivity to inhibition by pain and/or morphine was statistically significant (Fisher's exact probability test, P less than 0.01). Naloxone attenuated the inhibitory effects of both pain and morphine, thus suggesting mediation of both by the same neuronal mechanism. From this evidence we conclude that LHA glucose-sensitive neurons are involved in the suppression of feeding by noxious stimulation.