Thematische Bibliographien / Afferent pathways

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Auswahl der wissenschaftlichen Literatur zum Thema „Afferent pathways“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 1. August 2024

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Zeitschriftenartikel zum Thema "Afferent pathways"

Sun, Shu-Yu, Wei Wang, and Harold D. Schultz. "Activation of cardiac afferents by arachidonic acid: relative contributions of metabolic pathways." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 1 (July 1, 2001): H93—H104. http://dx.doi.org/10.1152/ajpheart.2001.281.1.h93.

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Arachidonic acid (AA) is metabolized via cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P-450 (CP450) pathways to a variety of bioactive products. The sensitivity of cardiac afferent endings to AA and its metabolites, especially those derived from LOX and CP450 pathways, is currently unclear. We examined AA-induced activation of cardiac vagal chemosensitive afferents in non- and postischemic hearts in rats and evaluated the relative contributions of the three metabolic pathways to the effects. Epicardial application of AA activated the cardiac afferents dose dependently in both nonischemic and postischemic hearts, with afferent responses greater in the latter condition. In nonischemic hearts, the afferent response to AA was abolished only after simultaneous administration of indomethacin and 17-octadecynoic acid (COX and CP450 inhibitors, respectively). Nordihydroguaiaretic acid (a LOX inhibitor) had no effect on the afferent response to AA. In postischemic hearts, abolition of the afferent response to AA required simultaneous blockade of all three pathways. None of the AA metabolic inhibitors affected resting activity of cardiac afferents in nonischemic hearts, but each suppressed afferent activity during ischemia-reperfusion. Most COX metabolites, CP450 metabolites, and 5-LOX metabolites tested were capable of activating cardiac afferents. The 12-LOX metabolites and 15-LOX metabolites had no effect on afferent activity. These data indicate that in the nonischemic heart, basal AA metabolism does not contribute to resting afferent activity, but AA is capable of activating cardiac afferents via COX and CP450 but not LOX pathways. During ischemia-reperfusion, all three metabolic pathways contribute to activation of cardiac vagal afferents with an enhanced responsiveness to AA. Our results suggest that induction of the 5-LOX pathway contributes to the enhanced sensitivity of cardiac vagal afferents to AA in the ischemic condition.

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Nelson, David W., James W. Sharp, Mark S. Brownfield, Helen E. Raybould, and Denise M. Ney. "Localization and Activation of Glucagon-Like Peptide-2 Receptors on Vagal Afferents in the Rat." Endocrinology 148, no. 5 (May 1, 2007): 1954–62. http://dx.doi.org/10.1210/en.2006-1232.

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Glucagon-like peptide-2 (GLP-2) is a nutrient-dependent proglucagon-derived hormone that stimulates intestinal growth through poorly understood paracrine and/or neural pathways. The relationship between GLP-2 action and a vagal pathway is unclear. Our aims were to determine whether 1) the GLP-2 receptor (GLP-2R) is expressed on vagal afferents by localizing it to the nodose ganglia; 2) exogenous GLP-2 stimulates the vagal afferent pathway by determining immunoreactivity for c-fos protein in the nucleus of the solitary tract (NTS); and 3) functional ablation of vagal afferents attenuates GLP-2-mediated intestinal growth in rats maintained with total parenteral nutrition (TPN). A polyclonal antibody against the N terminus of the rat GLP-2R was raised and characterized. The GLP-2R was localized to vagal afferents in the nodose ganglia and confirmed in enteroendocrine cells, enteric neurons, and nerve fibers in the myenteric plexus using immunohistochemistry. Activation of the vagal afferent pathway, as indicated by c-fos protein immunoreactivity in the NTS, was determined by immunohistochemistry after ip injection of 200 μg human GLP-2. GLP-2 induced a significant 5-fold increase in the number of c-fos protein immunoreactive neurons in the NTS compared with saline. Ablation of vagal afferent function by perivagal application of capsaicin, a specific afferent neurotoxin, abolished c-fos protein immunoreactivity, suggesting that activation of the NTS due to GLP-2 is dependent on vagal afferents. Exogenous GLP-2 prevented TPN-induced mucosal atrophy, but ablation of vagal afferent function with capsaicin did not attenuate this effect. This suggests that vagal-independent pathways are responsible for GLP-2 action in the absence of luminal nutrients during TPN, possibly involving enteric neurons or endocrine cells. This study shows for the first time that the GLP-2R is expressed by vagal afferents, and ip GLP-2 activates the vagal afferent pathway.

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Xu, Linjing, and G. F. Gebhart. "Characterization of Mouse Lumbar Splanchnic and Pelvic Nerve Urinary Bladder Mechanosensory Afferents." Journal of Neurophysiology 99, no. 1 (January 2008): 244–53. http://dx.doi.org/10.1152/jn.01049.2007.

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Sensory information from the urinary bladder is conveyed via lumbar splanchnic (LSN) and sacral pelvic (PN) nerves to the spinal cord. In the present report we compared the mechanosensitive properties of single afferent fibers in these two pathways using an in vitro mouse bladder preparation. Mechanosensitive primary afferents were recorded from the LSN or PN and distinguished based on their response to receptive field stimulation with different mechanical stimuli: probing (160 mg to 2 g), stretch (1–25 g), and stroking of the urothelium (10–1,000 mg). Four different classes of afferent were recorded from the LSN and PN: serosal, muscular, muscular/urothielial, and urothelial. The LSN contained principally serosal and muscular afferents (97% of the total sample), whereas all four afferent classes of afferent were present in the PN (63% of which were muscular afferents). In addition, the respective proportions and receptive field distributions differed between the two pathways. Both low- and high-threshold stretch-sensitive muscular afferents were present in both pathways, and muscular afferents in the PN were shown to sensitize after exposure to an inflammatory soup cocktail. The LSN and PN pathways contain different populations of mechanosensitive afferents capable of detecting a range of mechanical stimuli and individually tuned to detect the type, magnitude, and duration of the stimulus. This knowledge broadens our understanding of the potential roles these two pathways play in conveying mechanical information from the bladder to the spinal cord.

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Kirk, M. D. "Presynaptic inhibition in the crayfish CNS: pathways and synaptic mechanisms." Journal of Neurophysiology 54, no. 5 (November 1, 1985): 1305–25. http://dx.doi.org/10.1152/jn.1985.54.5.1305.

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I studied the pathways that produce primary afferent depolarization (PAD) and presynaptic inhibition during crayfish escape behavior. Simultaneous intracellular recordings were obtained from interneurons and primary afferent axons in the neuropil of the sixth abdominal ganglion. In several experiments, a sucrose-gap recording of PAD accompanied the intracellular impalements. I have identified PAD-producing inhibitory interneurons (PADIs) that are fired by a single impulse in the lateral (LG) or medial (MG) giant, escape-command axons; the PADIs appear to be directly responsible for presynaptic inhibition of primary afferent input to identified mechanosensory interneurons. PADI spikes, elicited by injection of depolarizing current, produced unitary PAD with constant short latency (mean = 0.97 +/- 0.12 SD ms). The unitary PADs were capable of following PADI impulses one for one at frequencies greater than 100 Hz, and the amplitude of unitary PAD was increased by injection of chloride into the afferent terminals. Therefore, the PADIs appear to directly produce an increase in chloride conductance in the primary afferent terminals. Intracellular injections of Lucifer yellow or horseradish peroxidase (HRP) revealed three morphological types of PADI. Their axonal branches and terminals are bilateral and overlap extensively with the innervation fields of all 10 sensory roots of the sixth ganglion. The three morphological types of PADI were physiologically indistinguishable. In several cases, the impaled PADI was shown to produce unitary PAD in more than one afferent of a given root as well as in afferents of adjacent roots. Therefore, the PADIs appear to diverge widely and contact many afferents in all of the sixth-ganglion sensory roots. Stimulation, caudal to the fifth ganglion, of an MG that had been interrupted rostral to the fifth ganglion produced no PAD in sixth-ganglion afferents. Also, stimulation of an MG or an LG in a surgically isolated sixth abdominal ganglion failed to produce PAD. Therefore, the pathway between the MGs and PADIs is activated exclusively within the rostral abdominal ganglia. Direct stimulation in the second and third abdominal ganglia of the segmental giants (SGs) produced a polysynaptic, suprathreshold response in the PADIs. This response was compound and was not due to the activity of the identified corollary discharge interneurons, CDI-2 and CDI-3, that are fired by the SGs. Therefore, the primary input to the PADIs must come from other, unidentified CDIs that are driven by the SGs. PADIs were not fired by shocks to the sensory portions of any peripheral roots even though these shocks produced PAD.(ABSTRACT TRUNCATED AT 400 WORDS)

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Friemert, B., S. Franke, A. Gollhofer, L. Claes, and M. Faist. "Group I Afferent Pathway Contributes to Functional Knee Stability." Journal of Neurophysiology 103, no. 2 (February 2010): 616–22. http://dx.doi.org/10.1152/jn.00172.2009.

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The hamstring reflex response has been suggested to play a substantial role in knee joint stabilization during anterior tibial translation. The present study was performed to determine which afferent pathways contribute to the hamstring reflex as well as the potential effects of specific afferent pathways on functional knee stability. Short- and medium-latency hamstring reflexes (SLR and MLR) were evoked by anterior tibial translation in 35 healthy subjects during standing with 30° knee flexion. Nerve cooling, tizanidine, and ischemia were employed to differentiate afferent pathways. Two hours of thigh cooling ( n = 10) resulted in a significant increase in MLR latency and, to a lesser extent, SLR latency. No significant changes were recorded in reflex sizes or maximum tibial translation. The ingestion of tizanidine ( n = 10), a suppressor of group II afferents, strongly reduced the MLR size while SLR size or latency of both reflex responses was not significantly affected. Maximum tibial translation was unchanged [5.3 ± 1.9 to 4.8 ± 2 (SD) mm; P = 0.410]. Ischemia in the thigh ( n = 15) led to a highly significant depression in SLR size (89 ± 4%; P < 0.001) but only a slight and not significant decline of MLR size. In these subjects maximum tibial translation increased significantly (6.9 ± 1.6 to 9.4 ± 3.2 mm; P = 0.028). It is concluded that the hamstring SLR is mediated by Ia afferents, while group II afferents mainly contribute to the MLR. Suppression of SLR may increase maximum anterior tibial translation, thus indicating a possible functional role of Ia afferents in knee joint stabilization.

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Liu, C. Y., M. H. Mueller, D. Grundy, and M. E. Kreis. "Vagal modulation of intestinal afferent sensitivity to systemic LPS in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 5 (May 2007): G1213—G1220. http://dx.doi.org/10.1152/ajpgi.00267.2006.

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The central nervous system modulates inflammation in the gastrointestinal tract via efferent vagal pathways. We hypothesized that these vagal efferents receive synaptic input from vagal afferents, representing an autonomic feedback mechanism. The consequence of this vagovagal reflex for afferent signal generation in response to LPS was examined in the present study. Different modifications of the vagal innervation or sham procedures were performed in anesthetized rats. Extracellular mesenteric afferent nerve discharge and systemic blood pressure were recorded in vivo before and after systemic administration of LPS (6 mg/kg iv). Mesenteric afferent nerve discharge increased dramatically following LPS, which was unchanged when vagal efferent traffic was eliminated by acute vagotomy. In chronically vagotomized animals, to eliminate both vagal afferent and efferent traffic, the increase in afferent firing 3.5 min after LPS was reduced to 3.2 ± 2.5 impulses/s above baseline compared with 42.2 ± 2.0 impulses/s in controls ( P < 0.001). A similar effect was observed following perivagal capsaicin, which was used to eliminate vagal afferent traffic only. LPS also caused a transient hypotension (<10 min), a partial recovery, and then persistent hypertension that was exacerbated by all three procedures. Mechanosensitivity was increased 15 min following LPS but had recovered at 30 min in all subgroups except for the chronic vagotomy group. In conclusion, discharge in capsaicin-sensitive mesenteric vagal afferents is augmented following systemic LPS. This activity, through a vagovagal pathway, helps to attenuate the effects of septic shock. The persistent hypersensitivity to mechanical stimulation after chronic vagal denervation suggests that the vagus exerts a regulatory influence on spinal afferent sensitization following LPS.

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Mazzone, Stuart B., and Bradley J. Undem. "Vagal Afferent Innervation of the Airways in Health and Disease." Physiological Reviews 96, no. 3 (July 2016): 975–1024. http://dx.doi.org/10.1152/physrev.00039.2015.

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Vagal sensory neurons constitute the major afferent supply to the airways and lungs. Subsets of afferents are defined by their embryological origin, molecular profile, neurochemistry, functionality, and anatomical organization, and collectively these nerves are essential for the regulation of respiratory physiology and pulmonary defense through local responses and centrally mediated neural pathways. Mechanical and chemical activation of airway afferents depends on a myriad of ionic and receptor-mediated signaling, much of which has yet to be fully explored. Alterations in the sensitivity and neurochemical phenotype of vagal afferent nerves and/or the neural pathways that they innervate occur in a wide variety of pulmonary diseases, and as such, understanding the mechanisms of vagal sensory function and dysfunction may reveal novel therapeutic targets. In this comprehensive review we discuss historical and state-of-the-art concepts in airway sensory neurobiology and explore mechanisms underlying how vagal sensory pathways become dysfunctional in pathological conditions.

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Webster, W. Andrew, and Michael J. Beyak. "The long chain fatty acid oleate activates mouse intestinal afferent nerves in vitro." Canadian Journal of Physiology and Pharmacology 91, no. 5 (May 2013): 375–79. http://dx.doi.org/10.1139/cjpp-2012-0138.

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Vagal afferents innervating the gastrointestinal tract serve an important nutrient-sensing function, and these signals contribute to satiety. Detection of nutrients occurs largely through the release of mediators from specialized enteroendocrine cells within the mucosa of the gastrointestinal tract. The signaling pathways leading to vagal afferent activation are not clear; however, previous in-vivo studies have implicated a role for cholecystokinin (CCK). We used an in vitro intestinal afferent extracellular recording preparation to study the effect of luminal perfusion of the long chain fatty acid oleate on mouse intestinal afferent activity. Oleate activated intestinal afferents in a concentration-dependent fashion, with an EC50 value of approximately 25 mmol/L. The L-type calcium channel blocker nicardipine attenuated the effect of oleate. Vagotomy resulted in a significant (>60%) reduction of the responses to both oleate and CCK. The CCK-1 receptor antagonist lorglumide nearly abolished responses to CCK and oleate. Our experiments therefore suggest that oleate activates intestinal afferents, with vagal afferents primarily involved; however, nonvagal fibres also contribute. The activation is dependent on CCK release, likely via activation of L-type channels on mucosal enteroendocrine cells, finally resulting in activation of CCK-1 receptors on the afferent terminals.

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Joris, Philip X., and Tom C. T. Yin. "Envelope Coding in the Lateral Superior Olive. III. Comparison With Afferent Pathways." Journal of Neurophysiology 79, no. 1 (January 1, 1998): 253–69. http://dx.doi.org/10.1152/jn.1998.79.1.253.

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Joris, Philip X. and Tom C. T. Yin. Envelope coding in the lateral superior olive. III. Comparison with afferent pathways. J. Neurophysiol. 79: 253–269, 1998. Binaural cues for spatial localization of complex high-frequency sounds are interaural level and time differences (ILDs and ITDs). We previously showed that cells in the lateral superior olive (LSO) are sensitive to ITDs in the envelope of sinusoidally amplitude-modulated (AM) signals up to a modulation frequency of only ∼800 Hz. To understand the limitations in this ITD-sensitivity, we here compare responses to monaural modulation in LSO and its input pathways, derived from cochlear nucleus and medial nucleus of the trapezoid body. These pathways have marked functional and morphological specializations, suggestive of adaptations for timing. Afferent cell populations were identified on the basis of electrophysiological signatures, and for each population, average firing rate and synchronization to AM tones were compared with auditory-nerve fibers and LSO cells. Except for an increase in modulation gain in some subpopulations, synchronization of LSO afferents was very similar to that in auditory nerve fibers in its dependency on sound pressure level (SPL), modulation depth, and modulation frequency. Distributions of cutoff frequencies of modulation transfer functions were largely coextensive with the distribution in auditory nerve. Group delays, measured from the phase of the response modulation as a function of modulation frequency, showed an orderly dependence on characteristic frequency and cell type and little dependence on SPL. Similar responses were obtained to a modulated broadband carrier. Compared with their afferents, LSO cells synchronized to monaurally modulated stimuli with a higher gain but often over a narrower range of modulation frequencies. Considering the scatter in afferent and LSO cell populations, ipsi- and contralateral responses were well matched in cutoff frequency and magnitude of delays. In contrast to their afferents, LSO cells show a decrease in average firing rate at high modulation frequencies. We conclude that the restricted modulation frequency range over which LSO cells show ITD-sensitivity does not result from loss of envelope information along the afferent pathway but is due to convergence or postsynaptic effects at the level of the LSO. The faithful transmission of envelope phase-locking in LSO afferents is consistent with their physiological and morphological adaptations, but these adaptations are not commensurate with the rather small effects of physiological ITDs reported previously, especially when compared with effects of ILDs. We suggest that these adaptations have evolved to allow a comparison of instantaneous amplitude fluctuations at the two ears rather than to extract interaural timing information per se.

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Ryan, Stephen, and Philip Nolan. "Superior laryngeal and hypoglossal afferents tonically influence upper airway motor excitability in anesthetized rats." Journal of Applied Physiology 99, no. 3 (September 2005): 1019–28. http://dx.doi.org/10.1152/japplphysiol.00776.2004.

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Upper airway (UA) muscle activity is stimulated by changes in UA transmural pressure and by asphyxia. These responses are reduced by muscle relaxation. We hypothesized that this is due to a change in afferent feedback in the ansa hypoglossi and/or superior laryngeal nerve (SLN). We examined 1) the glossopharyngeal motor responses to UA transmural pressure and asphyxia and 2) how these responses were changed by muscle relaxation in animals where one or both of these afferent pathways had been sectioned bilaterally. Experiments were performed in 24 anesthetized, thoracotomized, artificially ventilated rats. Baseline glossopharyngeal activity and its response to UA transmural pressure and asphyxia were moderately reduced after bilateral section of the ansa hypoglossi ( P < 0.05). Conversely, bilateral SLN section increased baseline glossopharyngeal activity, augmented the response to asphyxia, and abolished the response to UA transmural pressure. Muscle relaxation reduced resting glossopharyngeal activity and the response to asphyxia ( P < 0.001). This occurred whether or not the ansa hypoglossi, the SLN, or both afferent pathways had been interrupted. We conclude that ansa hypoglossi afferents tonically excite and SLN afferents tonically inhibit UA motor activity. Muscle relaxation depressed UA motor activity after section of the ansa hypoglossi and SLN. This suggests that some or all of the response to muscle relaxation is mediated by alterations in the activity of afferent fibers other than those in the ansa hypoglossi or SLN.

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Dissertationen zum Thema "Afferent pathways"

Roy, Sujata. "Segregation within afferent pathways in primate vision." Connect to thesis, 2009. http://repository.unimelb.edu.au/10187/4913.

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The current knowledge of the visual pathways in primates includes the patterns of projection from the retina through the dorsal lateral geniculate nucleus (dLGN) to the striate cortex (V1) and the extra-striate projections towards the dorsal and ventral streams. Cells with short wavelength sensitive cone (S-cone) inputs in the dLGN have been studied extensively in New World marmosets but not in Old World macaques. This thesis presents results from studies in the macaque monkey which are more relevant to humans since humans are closer in evolution to Old World than New World monkeys. The spatial, temporal, chromatic and orientation preferences of neurons in the dLGN of the macaque were investigated by electrophysiological methods. The physiological findings of cells with S-cone inputs were compared to cells with opponent inputs from the long and medium wavelength sensitive cones (L-cones & M-cones, respectively). The cells receiving S-cone inputs (blue-yellow or B-Y cells) preferred lower spatial frequencies than the cells with opponent L-cone and M-cone inputs (red-green or R-G cells). Orthodromic latencies from optic chiasm stimulation were measured where possible to distinguish differences in conduction velocity between the cell groups. Although the B-Y cells usually had longer latencies than R-G cells, there wasconsiderable overlap between the cell groups. The recorded cells were localised through histological reconstruction of dLGN sections stained for Nissl substance. The distribution of B-Y cells within the dLGN was compared to the distribution of R-G cells. The majority of B-Y cells were located within the intercalated koniocellular layers as well as the koniocellular bridges (extensions of the koniocellular layers into the adjacent parvocellular layers). The B-Y cells were also largely segregated within the middle dLGN layers (K3, P3, K4 & P4). The R-G cells were mainly concentrated within the parvocellular layers (P3, P4, P5 & P6) and were evenly distributed throughout the middle and outer layers of the dLGN. The study also included recordings from the extra-striate middle temporal area (MT) to determine whether a fast S-cone input exists from the dLGN to area MT which bypasses V1. The pattern of cone inputs to area MT neurons was investigated before and during inactivation of V1. The inactivation was done through reversible cooling with a Peltier thermocouple device or focal inactivation with y-amino butyric acid (GABA) iontophoresis. Precise inactivation of V1 to the topographically matching visual fields of the recording sites in area MT revealed a preservation of all three coneinputs in many cells. The subcortical sources of these preserved inputs are discussed with their relevance to blindsight, which is the limited retention of visual perception after V1 damage. Analysis of the latencies of area MT cells revealed a rough segregation into latencies faster or slower than 70 ms. Cells both with and without a significant change in response during V1 inactivation were present in each group. The findings reported in this thesis indicate that some of the preserved inputs in area MT during V1 inactivation may be carried by a direct input from the dLGN which bypasses V1.

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Gibson, Claire. "Interactions between afferent pathways in spinal cord development." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311132.

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Grillner, Pernilla. "Afferent input to midbrain dopamine neurones and its modulation : an electrophysiological study in vitro /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3712-5/.

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Needle, Alan R. "Microneurography evaluation of somatosensory afferent traffic in the unstable ankle." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 103 p, 2009. http://proquest.umi.com/pqdweb?did=1889099101&sid=2&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Lynn, Penelope Ann. "An electrophysiological investigation of colonic afferent sensitivity in the rat and mouse - in vitro /." Title page, contents and general abstract only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phl989.pdf.

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Zhang, Yongkui. "Functional development of otolith afferents in postnatal rats." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23295089.

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張永魁 and Yongkui Zhang. "Functional development of otolith afferents in postnatal rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31242716.

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Bulmer, David Colin Eric. "Central pathways activated by cardiac vagal afferent fibres in the rat." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.400590.

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Zheng, Fashan. "Baroreceptors and cardiopulmonary reflexes : afferent pathways and the influence of cold." Thesis, University of Aberdeen, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262348.

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A study was performed on decerebrate ferrets to define the contribution of vagal afferent non-myelinated fibres to the baroreceptor heart rate reflex produced by bolus i.v. injection of phenylephrine, using capsaicin as a selective C fibre blocker. Capsaicin blocked pulmonary chemoreflex substantially without any effects on bradycardia evoked by electrical stimulation of vagal efferent fibres to the heart. The significance of the contribution to bradycardia in response to marked increases in blood pressure by vagal C fibres are discussed in relation to findings in electrophysiological studies. A further study was performed on decerebrate ferrets and chloralose anaesthetised lambs. Baroreflex sensitivity was assessed by the relationship between cardiac interval changes and a rise in systolic blood pressure produced by bolus injection of phenylephrine and descending aorta occlusion. Moderate hypothermia (30-34oC) enhanced the baroreflex heart rate reflex substantially and was without effect on the sensitivity of pulmonary J receptor reflex pathways involved in the heart rate control. Action of vagal efferent fibres in altering heart rate was increased by moderate cooling. Such an effect may be partially responsible for the enhanced heart rate component of baroreflex response. Other possible mechanisms of enhanced baroreflex sensitivity are discussed. The consequence of enhanced vagal efferent fibre on heart was studied by electrical stimulation of the peripheral end of cervical vagus nerves in decerebrate ferrets and anaesthetised lambs. Moderate cooling substantially increases cardiac arrhythmias, such as sinus bradycardia, sinoatrial block, sinus arrest and A-V block. In addition vagal stimulation resulted in lethal ventricular arrythmia during infusion of noradrenaline. The possible mechanisms underlying the collapse and sudden death following rescue are discussed.

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Mariano, Timothy Yu. "Electrical Stimulation of Afferent Neural Pathways for Suppression of Urethral Reflexes." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1246392300.

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Bücher zum Thema "Afferent pathways"

J, Allum J. H., and Hulliger M, eds. Afferent control of posture and locomotion. Amsterdam: Elsevier, 1989.

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Taylor, David C. M. Nociceptive afferent neurones. Manchester: Manchester University Press, 1991.

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F, Fanardzhi͡a︡n V., ed. Vist͡s︡erosomaticheskie afferentnye sistemy gipotalamusa. Leningrad: Izd-vo "Nauka," Leningradskoe otd-nie, 1985.

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O, Pompeiano, and Allum J. H. J, eds. Vestibulospinal control of posture and locomotion. Amsterdam: Elsevier, 1988.

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A, Lenz Frederick, ed. The human pain system: Experimental and clinical perspectives. Cambridge: Cambridge University Press, 2010.

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Fred, Lenz, ed. The human pain system: Experimental and clinical perspectives. Cambridge: Cambridge University Press, 2010.

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Falk Symposium (103 1997 Freiburg, Germany). Liver and nervous system: Proceedings of the Falk Symposium 103 (Part III of the Liver Week in Freiburg 1997) held in Freiburg, Germany, October 4-5, 1997. Dordrecht: Kluwer Academic Publishers, 1998.

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N, Andrianov I͡U︡, ed. Sensory hair cells: Synaptic transmission. Berlin: Springer-Verlag, 1993.

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Ruffa, Geraldine Skuches. Afferent connections to the prefrontal cortex of the cat: Differential fronto-limbic connectivity and manifestations of kindled epileptic foci. [New Haven: s.n.], 1988.

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Ivanovich, Konstantinov Alekseĭ, ed. Fiziologii͡a︡ i biofizika sensornykh sistem: Mezhvuzovskiĭ sbornik. Leningrad: Izd-vo Leningradskogo universiteta, 1990.

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Buchteile zum Thema "Afferent pathways"

Choudhury, Eileen, Sumayya J. Almarzouqi, Michael L. Morgan, and Andrew G. Lee. "Afferent Visual Pathways." In Encyclopedia of Ophthalmology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-35951-4_1148-1.

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Choudhury, Eileen, Sumayya J. Almarzouqi, Michael L. Morgan, and Andrew G. Lee. "Afferent Visual Pathways." In Encyclopedia of Ophthalmology, 48–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_1148.

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de Groat, W. C. "Neuropeptides in pelvic afferent pathways." In Experientia Supplementum, 334–61. Basel: Birkhäuser Basel, 1989. http://dx.doi.org/10.1007/978-3-0348-9136-3_18.

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Dubner, Ronald, M. Catherine Bushnell, and Gary H. Duncan. "Sensory-Discriminative Capacities of Nociceptive Pathways and Their Modulation by Behavior." In Spinal Afferent Processing, 331–44. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-4994-5_13.

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Ádám, György. "Visceral Afferent Pathways and Central Projections." In Visceral Perception, 57–69. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4757-2903-0_6.

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Vierck, Charles J., Joel D. Greenspan, Louis A. Ritz, and David C. Yeomans. "The Spinal Pathways Contributing to the Ascending Conduction and the Descending Modulation of Pain Sensations and Reactions." In Spinal Afferent Processing, 275–329. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-4994-5_12.

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Read, Heather L., and Alex D. Reyes. "Sensing Sound Through Thalamocortical Afferent Architecture and Cortical Microcircuits." In The Mammalian Auditory Pathways, 169–98. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-71798-2_7.

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Lin, Haodong, and Chunlin Hou. "Reconstruction of Afferent and Efferent Nerve Pathways of the Atonic Bladder." In Functional Bladder Reconstruction Following Spinal Cord Injury via Neural Approaches, 83–91. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-7766-8_9.

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Hale, Matthew W., Graham A. W. Rook, and Christopher A. Lowry. "Pathways Underlying Afferent Signaling of Bronchopulmonary Immune Activation to the Central Nervous System." In Chemical Immunology and Allergy, 118–41. Basel: S. KARGER AG, 2012. http://dx.doi.org/10.1159/000336505.

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Dideriksen, Jakob Lund, Silvia Muceli, Strahinja Dosen, and Dario Farina. "Physiological Recruitment of Large Populations of Motor Units Using Electrical Stimulation of Afferent Pathways." In Biosystems & Biorobotics, 351–59. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08072-7_55.

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Konferenzberichte zum Thema "Afferent pathways"

Barbur, John L., Vicky A. Cole, J. A. Harlow, and Ivor S. Levy. "Isolation of Pupil Light Reflex Response Components: Selective Loss of Function in a Subject with Optic Nerve Drusen." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1996. http://dx.doi.org/10.1364/vsia.1996.thc.4.

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The ambient light level determines largely the steady-state size of the pupil (Lowenstein et al, 1964) and rapid increments in light flux on the retina cause a brisk constriction of the pupil that is often described as the dynamic light reflex response (Alexandridis, 1985; Lowenfeld, 1993). The afferent pathways that control the steady-state size of the pupil and the dynamic light reflex response in man have been associated with subcortical projections and this is consistent with clinical observations which suggest that the pupils continue to respond normally to sudden changes in room illumination even when the patients are cortically blind (Brindley et al, 1969). It is of great interest to investigate whether the same afferent pathway controls both the steady-state and the dynamic light reflex response in man. Analysis of pupil response curves measured as a function of luminance contrast when long duration stimuli are employed suggests that two independent principal components are sufficient to account for the family of curves that describe the observed pupil responses. These components have been labelled sustained and transient (Young et al, 1993; Young & Kennis, 1993). A number of pupil studies have demonstrated the absence of Pupil Light Reflex (PLR) responses in patients with post-geniculate lesions when small test stimuli are employed (Harms, 1951; Cibis et al, 1975; Barbur et al, 1988; Kardon, 1992; Kardon et al, 1993). Such observations suggest that more than one afferent pathway is involved in the control of the pupil response to light and that these pathways may not be entirely subcortical. A better understanding of the visual pathways involved and the kind of visual stimulus characteristics that cause pupillary responses will undoubtedly increase the usefulness of pupil based tests in neurologic and ophthalmologic examinations. With this in mind we have developed background perturbation techniques (Cole et al, 1995) that attempt to isolate different components of the PLR response. Preliminary findings are reported in normal subjects and in a patient with optic nerve drusen. The results suggest that the PLR is driven by at least two components. One component that integrates light flux changes over large areas of the visual field and determines largely the size of the pupil and a second component that dominates the response when small stimuli are involved and contributes significantly to the dynamic PLR response. This component is likely to be absent in patients with post-geniculate lesions.

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Cornsweet, Tom N. "Understanding the Swinging Flashlight Test of Pupil Function." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/navs.1991.md17.

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A large proportion of pathologies that affect the retina and visual pathways reduce a patient's sensitivity to light in one eye relative to the other. The swinging flashlight test, first described by Levatin (Arch. Ophthal. 62:768,1959) is a clinically useful way to detect such imbalances. The examiner shines a flashlight into one eye for a few seconds, then shifts abruptly to the other for a few seconds, and continues swinging back and forth while watching whichever eye is being illuminated. As reported by Levatin, when this test is performed on a normal visual system the pupils show little or no reaction because signals from each retina drive both pupils and shifting the same light from one retina to the other, then, should cause no change in the drive to either pupil. However, if the test is performed on a patient whose left retina, for example, is less sensitive than the right, then both pupils will constrict each time the right eye is illuminated and both will dilate each time the light shifts to the left eye. Such a result is called a Relative Afferent Pupillary Defect (RAPD). (It is relative because it will only appear if the sensitivities of the two eyes differ; it is afferent because, at least when considering a simplified model of the anatomy, it must result from an imbalance somewhere before the signals from the two eyes converge to drive both pupils.)

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Ambikairajah, Eliathamby, Owen Friel, and William Millar. "A speech recognition system using both auditory and afferent pathway signal processing." In 3rd International Conference on Spoken Language Processing (ICSLP 1994). ISCA: ISCA, 1994. http://dx.doi.org/10.21437/icslp.1994-386.

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Stewart, Barbara E., and Rockefeller S. L. Young. "Can The Pupillary Responses in Man Provide an Estimate of the Absolute Sensitivity of the Visual Pathway?" In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/navs.1988.tha2.

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Previous studies (Birch and Birch, 1987; Trejo and Cicerone, 1982; Schweizer, 1955) have used the pupillary light response to derive relative sensitivity estimates of the afferent visual pathway. The present study examines whether the pupillary response can provide an absolute sensitivity estimate. More specifically, this study addresses two questions: (i) Is a pupillary response elicited by flashes that are detected by the subject only 50% of the time? (ii) Does the pupil response occur on trials that the subject detects the flash, on trials that the subject does not detect the flash, or on both trials that are detected and not detected?

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