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Journal articles on the topic 'GABAergic/glycinergic synaptic transmission'

Author: Grafiati

Published: 6 June 2023

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1

Donato, Roberta, and Andrea Nistri. "Relative Contribution by GABA or Glycine to Cl−-Mediated Synaptic Transmission on Rat Hypoglossal Motoneurons In Vitro." Journal of Neurophysiology 84, no. 6 (2000): 2715–24. http://dx.doi.org/10.1152/jn.2000.84.6.2715.

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The relative contribution by GABA and glycine to synaptic transmission of motoneurons was investigated using an hypoglossus nucleus slice preparation from neonatal rats. Spontaneous, miniature, or electrically evoked postsynaptic currents (sPSCs, mPSCs, ePSCs, respectively) mediated by glycine or GABA were recorded under whole cell voltage clamp after blocking excitatory glutamatergic transmission with kynurenic acid. The overall majority of Cl−-mediated sPSCs was glycinergic, while only one-third was GABAergic; 70 ± 10% of mPSCs were glycinergic while 22 ± 8% were GABAergic. Tetrodotoxin (TTX

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2

Donato, Roberta, and Andrea Nistri. "Differential Short-Term Changes in GABAergic or Glycinergic Synaptic Efficacy on Rat Hypoglossal Motoneurons." Journal of Neurophysiology 86, no. 2 (2001): 565–74. http://dx.doi.org/10.1152/jn.2001.86.2.565.

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Using whole cell patch-clamp recording from hypoglossal motoneurons of a neonatal rat brain slice preparation, we investigated short-term changes in synaptic transmission mediated by GABA or glycine. In 1.5 mM extracellular Ca2+[Ca2+]o, pharmacologically isolated GABAergic or glycinergic currents were elicited by electrical stimulation of the reticular formation. At low stimulation frequency, glycinergic currents were larger and faster than GABAergic ones. GABAergic currents were strongly facilitated by pulse trains at 5 or 10 Hz without apparent depression. This phenomenon persisted after pha

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3

Awatramani, Gautam B., Rostislav Turecek, and Laurence O. Trussell. "Staggered Development of GABAergic and Glycinergic Transmission in the MNTB." Journal of Neurophysiology 93, no. 2 (2005): 819–28. http://dx.doi.org/10.1152/jn.00798.2004.

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Maturation of some brain stem and spinal inhibitory systems is characterized by a shift from GABAergic to glycinergic transmission. Little is known about how this transition is expressed in terms of individual axonal inputs and synaptic sites. We have explored this issue in the rat medial nucleus of the trapezoid body (MNTB). Synaptic responses at postnatal days 5–7 (P5–P7) were small, slow, and primarily mediated by GABAA receptors. By P8–P12, an additional, faster glycinergic component emerged. At these ages, GABAA, glycine, or both types of receptors mediated transmission, even at single sy

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4

Sebe, Joy Y., Erika D. Eggers, and Albert J. Berger. "Differential Effects of Ethanol on GABAA and Glycine Receptor-Mediated Synaptic Currents in Brain Stem Motoneurons." Journal of Neurophysiology 90, no. 2 (2003): 870–75. http://dx.doi.org/10.1152/jn.00119.2003.

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Ethanol potentiates glycinergic synaptic transmission to hypoglossal motoneurons (HMs). This effect on glycinergic transmission changes with postnatal development in that juvenile HMs (P9–13) are more sensitive to ethanol than neonate HMs (P1–3). We have now extended our previous study to investigate ethanol modulation of synaptic GABAA receptors (GABAARs), because both GABA and glycine mediate inhibitory synaptic transmission to brain stem motoneurons. We tested the effects of ethanol on GABAergic and glycinergic miniature inhibitory postsynaptic currents (mIPSCs) recorded from neonate and ju

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5

Liu, Tao, Tsugumi Fujita, and Eiichi Kumamoto. "Acetylcholine and norepinephrine mediate GABAergic but not glycinergic transmission enhancement by melittin in adult rat substantia gelatinosa neurons." Journal of Neurophysiology 106, no. 1 (2011): 233–46. http://dx.doi.org/10.1152/jn.00838.2010.

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GABAergic and glycinergic inhibitory synaptic transmissions in substantia gelatinosa (SG; lamina II of Rexed) neurons of the spinal dorsal horn play an important role in regulating nociceptive transmission from the periphery. It has not yet been well known whether each of the inhibitory transmissions plays a distinct role in the regulation. We report an involvement of neurotransmitters in GABAergic but not glycinergic transmission enhancement produced by the PLA2 activator melittin, where the whole-cell patch-clamp technique is applied to the SG neurons of adult rat spinal cord slices. Glycine

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Schubert, Timm, Daniel Kerschensteiner, Erika D. Eggers, et al. "Development of Presynaptic Inhibition Onto Retinal Bipolar Cell Axon Terminals Is Subclass-Specific." Journal of Neurophysiology 100, no. 1 (2008): 304–16. http://dx.doi.org/10.1152/jn.90202.2008.

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Synaptic integration is modulated by inhibition onto the dendrites of postsynaptic cells. However, presynaptic inhibition at axonal terminals also plays a critical role in the regulation of neurotransmission. In contrast to the development of inhibitory synapses onto dendrites, GABAergic/glycinergic synaptogenesis onto axon terminals has not been widely studied. Because retinal bipolar cells receive subclass-specific patterns of GABAergic and glycinergic presynaptic inhibition, they are a good model for studying the development of inhibition at axon terminals. Here, using whole cell recording

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7

Liu, Tao, Tsugumi Fujita, Terumasa Nakatsuka, and Eiichi Kumamoto. "Phospholipase A2 Activation Enhances Inhibitory Synaptic Transmission in Rat Substantia Gelatinosa Neurons." Journal of Neurophysiology 99, no. 3 (2008): 1274–84. http://dx.doi.org/10.1152/jn.01292.2007.

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Phospholipase A2 (PLA2) activation enhances glutamatergic excitatory synaptic transmission in substantia gelatinosa (SG) neurons, which play a pivotal role in regulating nociceptive transmission in the spinal cord. By using melittin as a tool to activate PLA2, we examined the effect of PLA2 activation on spontaneous inhibitory postsynaptic currents (sIPSCs) recorded at 0 mV in SG neurons of adult rat spinal cord slices by use of the whole cell patch-clamp technique. Melittin enhanced the frequency and amplitude of GABAergic and glycinergic sIPSCs. The enhancement of GABAergic but not glycinerg

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8

Gao, Bao-Xi, Christian Stricker, and Lea Ziskind-Conhaim. "Transition From GABAergic to Glycinergic Synaptic Transmission in Newly Formed Spinal Networks." Journal of Neurophysiology 86, no. 1 (2001): 492–502. http://dx.doi.org/10.1152/jn.2001.86.1.492.

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The role of glycinergic and GABAergic systems in mediating spontaneous synaptic transmission in newly formed neural networks was examined in motoneurons in the developing rat spinal cord. Properties of action potential–independent miniature inhibitory postsynaptic currents (mIPSCs) mediated by glycine and GABAA receptors (GlyR and GABAAR) were studied in spinal cord slices of 17- to 18-day-old embryos ( E17–18) and 1- to 3-day-old postnatal rats ( P1–3). mIPSC frequency and amplitude significantly increased after birth, while their decay time decreased. To determine the contribution of glycine

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9

McMenamin, Caitlin A., Laura Anselmi, R. Alberto Travagli, and Kirsteen N. Browning. "Developmental regulation of inhibitory synaptic currents in the dorsal motor nucleus of the vagus in the rat." Journal of Neurophysiology 116, no. 4 (2016): 1705–14. http://dx.doi.org/10.1152/jn.00249.2016.

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Prior immunohistochemical studies have demonstrated that at early postnatal time points, central vagal neurons receive both glycinergic and GABAergic inhibitory inputs. Functional studies have demonstrated, however, that adult vagal efferent motoneurons receive only inhibitory GABAergic synaptic inputs, suggesting loss of glycinergic inhibitory neurotransmission during postnatal development. The purpose of the present study was to test the hypothesis that the loss of glycinergic inhibitory synapses occurs in the immediate postnatal period. Whole cell patch-clamp recordings were made from dorsa

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10

Shao, Mei, June C. Hirsch, and Kenna D. Peusner. "Emergence of Action Potential Generation and Synaptic Transmission in Vestibular Nucleus Neurons." Journal of Neurophysiology 96, no. 3 (2006): 1215–26. http://dx.doi.org/10.1152/jn.00180.2006.

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Principal cells of the chick tangential nucleus are vestibular nucleus neurons in the hindbrain. Although detailed information is available on the morphogenesis of principal cells and synaptogenesis of primary vestibular fibers, this is the first study of their early functional development, when vestibular terminals emerge at embryonic days 10 and 13 (E10 and E13). At E10, 60% of principal cells generated spikes on depolarization, whereas 50% exhibited excitatory postsynaptic currents (EPSCs) on vestibular-nerve stimulation. The frequency was 0.2 Hz for glutamatergic spontaneous EPSCs (sEPSCs)

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11

Reymond-Marron, I., M. Raggenbass, and M. Zaninetti. "Vasopressin facilitates glycinergic and GABAergic synaptic transmission in developing hypoglossal motoneurons." European Journal of Neuroscience 21, no. 6 (2005): 1601–9. http://dx.doi.org/10.1111/j.1460-9568.2005.03996.x.

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12

Sebe, Joy Y., Johannes F. van Brederode, and Albert J. Berger. "Inhibitory Synaptic Transmission Governs Inspiratory Motoneuron Synchronization." Journal of Neurophysiology 96, no. 1 (2006): 391–403. http://dx.doi.org/10.1152/jn.00086.2006.

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Neurons within the intact respiratory network produce bursts of action potentials that cause inspiration or expiration. Within inspiratory bursts, activity is synchronized on a shorter timescale to generate clusters of action potentials that occur in a set frequency range and are called synchronous oscillations. We investigated how GABA and glycine modulate synchronous oscillations and respiratory rhythm during postnatal development. We recorded inspiratory activity from hypoglossal nerves using the in vitro rhythmically active mouse medullary slice preparation from P0–P11 mice. Average oscill

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13

Kumamoto, Eiichi. "Cellular Mechanisms for Antinociception Produced by Oxytocin and Orexins in the Rat Spinal Lamina II—Comparison with Those of Other Endogenous Pain Modulators." Pharmaceuticals 12, no. 3 (2019): 136. http://dx.doi.org/10.3390/ph12030136.

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Much evidence indicates that hypothalamus-derived neuropeptides, oxytocin, orexins A and B, inhibit nociceptive transmission in the rat spinal dorsal horn. In order to unveil cellular mechanisms for this antinociception, the effects of the neuropeptides on synaptic transmission were examined in spinal lamina II neurons that play a crucial role in antinociception produced by various analgesics by using the whole-cell patch-clamp technique and adult rat spinal cord slices. Oxytocin had no effect on glutamatergic excitatory transmission while producing a membrane depolarization, γ-aminobutyric ac

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14

van Zundert, Brigitte, Patricio Castro, and Luis G. Aguayo. "Glycinergic and GABAergic synaptic transmission are differentially affected by gephyrin in spinal neurons." Brain Research 1050, no. 1-2 (2005): 40–47. http://dx.doi.org/10.1016/j.brainres.2005.05.014.

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15

Jin, Xiao-Tao, Ningren Cui, Weiwei Zhong, Xin Jin, Zhongying Wu та Chun Jiang. "Pre- and postsynaptic modulations of hypoglossal motoneurons by α-adrenoceptor activation in wild-type and Mecp2−/Y mice". American Journal of Physiology-Cell Physiology 305, № 10 (2013): C1080—C1090. http://dx.doi.org/10.1152/ajpcell.00109.2013.

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Hypoglossal motoneurons (HNs) control tongue movement and play a role in maintenance of upper airway patency. Defects in these neurons may contribute to the development of sleep apnea and other cranial motor disorders including Rett syndrome (RTT). HNs are modulated by norepinephrine (NE) through α-adrenoceptors. Although postsynaptic mechanisms are known to play a role in this effect, how NE modulates the synaptic transmissions of HNs remains poorly understood. More importantly, the NE system is defective in RTT, while how the defect affects HNs is unknown. Believing that information of NE mo

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16

Nakamura, Shiro, Tomio Inoue, Kan Nakajima, et al. "Synaptic Transmission From the Supratrigeminal Region to Jaw-Closing and Jaw-Opening Motoneurons in Developing Rats." Journal of Neurophysiology 100, no. 4 (2008): 1885–96. http://dx.doi.org/10.1152/jn.01145.2007.

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The supratrigeminal region (SupV) receives abundant orofacial sensory inputs and descending inputs from the cortical masticatory area and contains premotor neurons that target the trigeminal motor nucleus (MoV). Thus it is possible that the SupV is involved in controlling jaw muscle activity via sensory inputs during mastication. We used voltage-sensitive dye, laser photostimulation, patch-clamp recordings, and intracellular biocytin labeling to investigate synaptic transmission from the SupV to jaw-closing and jaw-opening motoneurons in the MoV in brain stem slice preparations from developing

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17

Medrihan, L., E. Tantalaki, G. Aramuni, et al. "Early Defects of GABAergic Synapses in the Brain Stem of a MeCP2 Mouse Model of Rett Syndrome." Journal of Neurophysiology 99, no. 1 (2008): 112–21. http://dx.doi.org/10.1152/jn.00826.2007.

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Rett syndrome is a neurodevelopmental disorder caused by mutations in the transcriptional repressor methyl-CpG-binding protein 2 (MeCP2) and represents the leading genetic cause for mental retardation in girls. MeCP2-mutant mice have been generated to study the molecular mechanisms of the disease. It was suggested that an imbalance between excitatory and inhibitory neurotransmission is responsible for the behavioral abnormalities, although it remained largely unclear which synaptic components are affected and how cellular impairments relate to the time course of the disease. Here, we report th

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18

Lu, Van B., William F. Colmers, and Peter A. Smith. "Long-term actions of BDNF on inhibitory synaptic transmission in identified neurons of the rat substantia gelatinosa." Journal of Neurophysiology 108, no. 2 (2012): 441–52. http://dx.doi.org/10.1152/jn.00457.2011.

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Peripheral nerve injury promotes the release of brain-derived neurotrophic factor (BDNF) from spinal microglial cells and primary afferent terminals. This induces an increase in dorsal horn excitability that contributes to “central sensitization” and to the onset of neuropathic pain. Although it is accepted that impairment of GABAergic and/or glycinergic inhibition contributes to this process, certain lines of evidence suggest that GABA release in the dorsal horn may increase after nerve injury. To resolve these contradictory findings, we exposed rat spinal cord neurons in defined-medium organ

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19

Fischl, Matthew J., Sonia R. Weimann, Michael G. Kearse, and R. Michael Burger. "Slowly emerging glycinergic transmission enhances inhibition in the sound localization pathway of the avian auditory system." Journal of Neurophysiology 111, no. 3 (2014): 565–72. http://dx.doi.org/10.1152/jn.00640.2013.

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Localization of low-frequency acoustic stimuli is processed in dedicated neural pathways where coincidence-detecting neurons compare the arrival time of sound stimuli at the two ears, or interaural time disparity (ITD). ITDs occur in the submillisecond range, and vertebrates have evolved specialized excitatory and inhibitory circuitry to compute these differences. Glycinergic inhibition is a computationally significant and prominent component of the mammalian ITD pathway. However, evidence for glycinergic transmission is limited in birds, where GABAergic inhibition has been thought to be the d

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20

Apostolides, Pierre F., and Laurence O. Trussell. "Chemical synaptic transmission onto superficial stellate cells of the mouse dorsal cochlear nucleus." Journal of Neurophysiology 111, no. 9 (2014): 1812–22. http://dx.doi.org/10.1152/jn.00821.2013.

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The dorsal cochlear nucleus (DCN) is a cerebellum-like auditory brain stem region whose functions include sound localization and multisensory integration. Although previous in vivo studies have shown that glycinergic and GABAergic inhibition regulate the activity of several DCN cell types in response to sensory stimuli, data regarding the synaptic inputs onto DCN inhibitory interneurons remain limited. Using acute DCN slices from mice, we examined the properties of excitatory and inhibitory synapses onto the superficial stellate cell, a poorly understood cell type that provides inhibition to D

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21

Sadlaoud, K., S. Tazerart, C. Brocard, et al. "Differential Plasticity of the GABAergic and Glycinergic Synaptic Transmission to Rat Lumbar Motoneurons after Spinal Cord Injury." Journal of Neuroscience 30, no. 9 (2010): 3358–69. http://dx.doi.org/10.1523/jneurosci.6310-09.2010.

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22

Kanjhan, Refik, Peter G. Noakes, and Mark C. Bellingham. "Emerging Roles of Filopodia and Dendritic Spines in Motoneuron Plasticity during Development and Disease." Neural Plasticity 2016 (2016): 1–31. http://dx.doi.org/10.1155/2016/3423267.

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Motoneurons develop extensive dendritic trees for receiving excitatory and inhibitory synaptic inputs to perform a variety of complex motor tasks. At birth, the somatodendritic domains of mouse hypoglossal and lumbar motoneurons have dense filopodia and spines. Consistent with Vaughn’s synaptotropic hypothesis, we propose a developmental unified-hybrid model implicating filopodia in motoneuron spinogenesis/synaptogenesis and dendritic growth and branching critical for circuit formation and synaptic plasticity at embryonic/prenatal/neonatal period. Filopodia density decreases and spine density

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23

Noguchi, Tsuyoshi, Shiro Nakamura, Kiyomi Nakayama, et al. "Developmental changes in GABAergic and glycinergic synaptic transmission to rat motoneurons innervating jaw-closing and jaw-opening muscles." Brain Research 1777 (February 2022): 147753. http://dx.doi.org/10.1016/j.brainres.2021.147753.

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24

Ziskind-Conhaim, Lea, Linying Wu, and Eric P. Wiesner. "Persistent Sodium Current Contributes to Induced Voltage Oscillations in Locomotor-Related Hb9 Interneurons in the Mouse Spinal Cord." Journal of Neurophysiology 100, no. 4 (2008): 2254–64. http://dx.doi.org/10.1152/jn.90437.2008.

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Neurochemically induced membrane voltage oscillations and firing episodes in spinal excitatory interneurons expressing the HB9 protein (Hb9 INs) are synchronous with locomotor-like rhythmic motor outputs, suggesting that they contribute to the excitatory drive of motoneurons during locomotion. Similar to central pattern generator neurons in other systems, Hb9 INs are interconnected via electrical coupling, and their rhythmic activity does not depend on fast glutamatergic synaptic transmission. The primary objective of this study was to determine the contribution of fast excitatory and inhibito

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Jiang, Chang-Yu, Tsugumi Fujita, and Eiichi Kumamoto. "Synaptic modulation and inward current produced by oxytocin in substantia gelatinosa neurons of adult rat spinal cord slices." Journal of Neurophysiology 111, no. 5 (2014): 991–1007. http://dx.doi.org/10.1152/jn.00609.2013.

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Cellular mechanisms for antinociception produced by oxytocin in the spinal dorsal horn have not yet been investigated thoroughly. We examined how oxytocin affects synaptic transmission in substantia gelatinosa neurons, which play a pivotal role in regulating nociceptive transmission, by applying the whole-cell patch-clamp technique to the substantia gelatinosa neurons of adult rat spinal cord slices. Bath-applied oxytocin did not affect glutamatergic spontaneous, monosynaptically-evoked primary-afferent Aδ-fiber and C-fiber excitatory transmissions. On the other hand, oxytocin produced an inwa

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Baba, Hiroshi, Koki Shimoji, and Megumu Yoshimura. "Norepinephrine Facilitates Inhibitory Transmission in Substantia Gelatinosa of Adult Rat Spinal Cord (Part 1)." Anesthesiology 92, no. 2 (2000): 473. http://dx.doi.org/10.1097/00000542-200002000-00030.

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Background The activation of descending norepinephrine-containing fibers from the brain stem inhibits nociceptive transmission at the spinal level. How these descending noradrenergic pathways exert the analgesic effect is not understood fully. Membrane hyperpolarization of substantia gelatinosa (Rexed lamina II) neurons by the activation of alpha2 receptors may account for depression of pain transmission. In addition, it is possible that norepinephrine affects transmitter release in the substantia gelatinosa. Methods Adult male Sprague-Dawley rats (9-10 weeks of age, 250-300 g) were used in th

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27

Shao, Xuesi M., and Jack L. Feldman. "Respiratory Rhythm Generation and Synaptic Inhibition of Expiratory Neurons in Pre-Bötzinger Complex: Differential Roles of Glycinergic and GABAergic Neural Transmission." Journal of Neurophysiology 77, no. 4 (1997): 1853–60. http://dx.doi.org/10.1152/jn.1997.77.4.1853.

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Shao, Xuesi M. and Jack L. Feldman. Respiratory rhythm generation and synaptic inhibition of expiratory neurons in pre-Bötzinger complex: differential roles of glycinergic and GABAergic neural transmission. J. Neurophysiol. 77: 1853–1860, 1997. A key distinction between neural pacemaker and conventional network models for the generation of breathing rhythm in mammals is whether phasic reciprocal inhibitory interactions between inspiratory and expiratory neurons are required. In medullary slices from neonatal rats generating respiratory-related rhythm, we measured the phasic inhibitory inputs t

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Dubuc, R�jean, Fulvia Bongianni, Yoshihiro Ohta, and Sten Grillner. "Dorsal root and dorsal column mediated synaptic inputs to reticulospinal neurons in lampreys: Involvement of glutamatergic, glycinergic, and GABaergic transmission." Journal of Comparative Neurology 327, no. 2 (1993): 251–59. http://dx.doi.org/10.1002/cne.903270207.

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29

El Khoueiry, Corinne, Cristina Alba-Delgado, Myriam Antri та ін. "GABAA and Glycine Receptor-Mediated Inhibitory Synaptic Transmission onto Adult Rat Lamina IIi PKCγ-Interneurons: Pharmacological but Not Anatomical Specialization". Cells 11, № 8 (2022): 1356. http://dx.doi.org/10.3390/cells11081356.

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Mechanical allodynia (pain to normally innocuous tactile stimuli) is a widespread symptom of inflammatory and neuropathic pain. Spinal or medullary dorsal horn (SDH or MDH) circuits mediating tactile sensation and pain need to interact in order to evoke mechanical allodynia. PKCγ-expressing (PKCγ+) interneurons and inhibitory controls within SDH/MDH inner lamina II (IIi) are pivotal in connecting touch and pain circuits. However, the relative contribution of GABA and glycine to PKCγ+ interneuron inhibition remains unknown. We characterized inhibitory inputs onto PKCγ+ interneurons by combining

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Yue, Hai-Yuan, Tsugumi Fujita, and Eiichi Kumamoto. "Biphasic modulation by galanin of excitatory synaptic transmission in substantia gelatinosa neurons of adult rat spinal cord slices." Journal of Neurophysiology 105, no. 5 (2011): 2337–49. http://dx.doi.org/10.1152/jn.00991.2010.

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Although intrathecally administrated galanin modulates nociceptive transmission in a biphasic manner, this has not been fully examined previously. In the present study, the action of galanin on synaptic transmission in the substantia gelatinosa (SG) neurons of adult rat spinal cord slices was examined, using the whole cell patch-clamp technique. Galanin concentration-dependently increased the frequency of spontaneous excitatory postsynaptic current (EPSC; EC50 = 2.0 nM) without changing the amplitude, indicating a presynaptic effect. This effect was reduced in a Ca2+-free, or voltage-gated Ca2

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Singh, Mandakini B., Jesse A. White, Eric J. McKimm, Milena M. Milosevic, and Srdjan D. Antic. "Mechanisms of Spontaneous Electrical Activity in the Developing Cerebral Cortex—Mouse Subplate Zone." Cerebral Cortex 29, no. 8 (2018): 3363–79. http://dx.doi.org/10.1093/cercor/bhy205.

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Abstract Subplate (SP) neurons exhibit spontaneous plateau depolarizations mediated by connexin hemichannels. Postnatal (P1–P6) mice show identical voltage pattern and drug-sensitivity as observed in slices from human fetal cortex; indicating that the mouse is a useful model for studying the cellular physiology of the developing neocortex. In mouse SP neurons, spontaneous plateau depolarizations were insensitive to blockers of: synaptic transmission (glutamatergic, GABAergic, or glycinergic), pannexins (probenecid), or calcium channels (mibefradil, verapamil, diltiazem); while highly sensitive

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Rozzo, Aldo, Laura Ballerini, Gilda Abbate, and Andrea Nistri. "Experimental and Modeling Studies of Novel Bursts Induced by Blocking Na+ Pump and Synaptic Inhibition in the Rat Spinal Cord." Journal of Neurophysiology 88, no. 2 (2002): 676–91. http://dx.doi.org/10.1152/jn.2002.88.2.676.

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This study addressed some electrophysiological mechanisms enabling neonatal rat spinal networks in vitro to generate spontaneous rhythmicity. Networks, made up by excitatory connections only after block of GABAergic and glycinergic transmission, develop regular bursting (disinhibited bursts) suppressed by the Na+ pump blocker strophanthidin. Thus the Na+ pump is considered important to control bursts. This study, however, shows that, after about 1 h in strophanthidin solution, networks of the rat isolated spinal cord surprisingly resumed spontaneous bursting (“strophanthidin bursting”), which

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Inquimbert, Perrine, Jean-Luc Rodeau, and Rémy Schlichter. "Differential contribution of GABAergic and glycinergic components to inhibitory synaptic transmission in lamina II and laminae III-IV of the young rat spinal cord." European Journal of Neuroscience 26, no. 10 (2007): 2940–49. http://dx.doi.org/10.1111/j.1460-9568.2007.05919.x.

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Narikawa, Keita, Hidemasa Furue, Eiichi Kumamoto, and Megumu Yoshimura. "In Vivo Patch-Clamp Analysis of IPSCs Evoked in Rat Substantia Gelatinosa Neurons by Cutaneous Mechanical Stimulation." Journal of Neurophysiology 84, no. 4 (2000): 2171–74. http://dx.doi.org/10.1152/jn.2000.84.4.2171.

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To know a functional role of inhibitory synaptic responses in transmitting noxious and innoxious information from the periphery to the rat spinal dorsal horn, we examined inhibitory postsynaptic currents (IPSCs) elicited in substantia gelatinosa (SG) neurons by mechanical stimuli applied to the skin using the newly developed in vivo patch-clamp technique. In the majority (80%) of SG neurons examined, a brush stimulus applied to the ipsilateral hind limb produced a barrage of IPSCs that persisted during the stimulus, while a pinch stimulus evoked IPSCs only at its beginning and end. The pinch-e

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van Brederode, Johannes F. M., and Albert J. Berger. "Spike-Firing Resonance in Hypoglossal Motoneurons." Journal of Neurophysiology 99, no. 6 (2008): 2916–28. http://dx.doi.org/10.1152/jn.01037.2007.

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During an inspiration the output of hypoglossal (XII) motoneurons (HMs) in vitro is characterized by synchronous oscillatory firing in the 20- to 40-Hz range. To maintain synchronicity it is important that the cells fire with high reliability and precision. It is not known whether the intrinsic properties of HMs are tuned to maintain synchronicity when stimulated with time-varying inputs. We intracellularly recorded from HMs in an in vitro brain stem slice preparation from juvenile mice. Cells were held at or near spike threshold and were stimulated with steady or swept sine-wave current funct

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Lewis, C. A., and D. S. Faber. "Inhibitory synaptic transmission in isolated patches of membrane from cultured rat spinal cord and medullary neurons." Journal of Neurophysiology 76, no. 1 (1996): 461–70. http://dx.doi.org/10.1152/jn.1996.76.1.461.

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1. To quantify the variability in the characteristics of inhibitory glycinergic and GABAergic currents at single synaptic connections between cultured rat embryonic spinal cord or medullary neurons, we have used patch-clamp techniques to record miniature inhibitory postsynaptic currents (mIPSCs) in cell-attached patches. Experiments were performed with the patch pipette containing either a low-calcium internal saline to allow comparison with subsequent whole cell recordings or external saline with tetrodotoxin, DL-2-amino-5-phosphonovaleric acid, and 6-cyano-7-nitroquinoxaline-2,3-dione, a sol

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Lewis, C. A., and D. S. Faber. "Properties of spontaneous inhibitory synaptic currents in cultured rat spinal cord and medullary neurons." Journal of Neurophysiology 76, no. 1 (1996): 448–60. http://dx.doi.org/10.1152/jn.1996.76.1.448.

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1. To identify the type(s) and properties of inhibitory postsynaptic receptor(s) involved in synaptic transmission in cultured rat embryonic spinal cord and medullary neurons, we have used whole cell patch-clamp techniques to record miniature inhibitory postsynaptic currents (mIPSCs) in the presence of tetrodotoxin, DL-2-amino-5-phosphonovaleric acid, and 6-cyano-7-nitroquinoxaline-2,3-dione. 2. The mIPSCs recorded from both spinal cord and medullary neurons had skewed amplitude distributions. 3. The glycinergic antagonist strychnine and the GABAergic antagonist bicuculline each decreased both

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Rudomin, P., I. Jimenez, J. Quevedo, and M. Solodkin. "Pharmacologic analysis of inhibition produced by last-order intermediate nucleus interneurons mediating nonreciprocal inhibition of motoneurons in cat spinal cord." Journal of Neurophysiology 63, no. 1 (1990): 147–60. http://dx.doi.org/10.1152/jn.1990.63.1.147.

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1. The aim of this study was to investigate the effects of drugs blocking glycinergic and GABAergic transmission on the postsynaptic inhibition of hindlimb motoneurons produced by activation of last-order laminae V-VI interneurons, which are coexcited by muscle and cutaneous afferents and have axonal branches projecting to the Clarke's column. 2. In anesthetized cats with right spinal cord hemisected and both dorsal columns cut between L4 and L5 segments, stimulation of the Clarke's column (CC) at L3-L4 level produced a short-latency, presumably monosynaptic, inhibitory potential that could be

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Wang, Jijiang, Xin Wang, Mustapha Irnaten, et al. "Endogenous Acetylcholine and Nicotine Activation Enhances GABAergic and Glycinergic Inputs to Cardiac Vagal Neurons." Journal of Neurophysiology 89, no. 5 (2003): 2473–81. http://dx.doi.org/10.1152/jn.00934.2002.

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The heart slows during expiration and heart rate increases during inspiration. This cardiorespiratory interaction is thought to occur by increased inhibitory synaptic events to cardiac vagal neurons during inspiration. Since cholinergic receptors have been suggested to be involved in this cardiorespiratory interaction, we tested whether endogenous cholinergic activity modulates GABAergic and glycinergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus, whether nicotine can mimic this facilitation, and we examined the nicotinic receptors involved. Cardiac vagal neurons in the

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Muller, Jay F., Josef Ammermüller, Richard A. Normann, and Helga Kolb. "Synaptic inputs to physiologically defined turtle retinal ganglion cells." Visual Neuroscience 7, no. 5 (1991): 409–29. http://dx.doi.org/10.1017/s0952523800009718.

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AbstractTwo physiologically distinct, HRP-marked turtle retinal ganglion cells were examined for their morphology, GABAergic, glycinergic, and bipolar cell synaptic inputs, using electron-microscopic autoradiography and postembedding immunocytochemistry. One cell was a color-opponent, transient ON/OFF ganglion cell. Its center response to red was a sustained hyperpolarization, and its center response to green was a depolarization with increased spiking at onset. The HRP-injected cell most resembled G6, from previous Golgi-impregnation studies (Kolb, 1982; Kolb et al., 1988). It was a narrow-fi

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Shimizu-Okabe, Chigusa, Shiori Kobayashi, Jeongtae Kim, et al. "Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord." International Journal of Molecular Sciences 23, no. 2 (2022): 834. http://dx.doi.org/10.3390/ijms23020834.

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Gamma-aminobutyric acid (GABA) and glycine act as inhibitory neurotransmitters. Three types of inhibitory neurons and terminals, GABAergic, GABA/glycine coreleasing, and glycinergic, are orchestrated in the spinal cord neural circuits and play critical roles in regulating pain, locomotive movement, and respiratory rhythms. In this study, we first describe GABAergic and glycinergic transmission and inhibitory networks, consisting of three types of terminals in the mature mouse spinal cord. Second, we describe the developmental formation of GABAergic and glycinergic networks, with a specific foc

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O’Brien, Jennifer A., and Albert J. Berger. "Cotransmission of GABA and Glycine to Brain Stem Motoneurons." Journal of Neurophysiology 82, no. 3 (1999): 1638–41. http://dx.doi.org/10.1152/jn.1999.82.3.1638.

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Using whole cell patch-clamp recording in a rat brain stem slice preparation, we found that γ-aminobutyric acid (GABA) and glycine act as cotransmitters to hypoglossal motoneurons (HMs). Focal application of GABA and glycine onto a single HM revealed that GABAAand glycine receptors are present on the same neuron. To demonstrate that HMs receive both GABAergic and glycinergic synaptic inputs, we simultaneously recorded GABAA- and glycine-receptor–mediated spontaneous miniature inhibitory postsynaptic currents (mIPSCs) in single HMs. GABAergic and glycinergic mIPSCs were differentiated based on

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Fogarty, Matthew J. "Inhibitory Synaptic Influences on Developmental Motor Disorders." International Journal of Molecular Sciences 24, no. 8 (2023): 6962. http://dx.doi.org/10.3390/ijms24086962.

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During development, GABA and glycine play major trophic and synaptic roles in the establishment of the neuromotor system. In this review, we summarise the formation, function and maturation of GABAergic and glycinergic synapses within neuromotor circuits during development. We take special care to discuss the differences in limb and respiratory neuromotor control. We then investigate the influences that GABAergic and glycinergic neurotransmission has on two major developmental neuromotor disorders: Rett syndrome and spastic cerebral palsy. We present these two syndromes in order to contrast th

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Betz, H., J. Gomeza, W. Armsen, P. Scholze, and V. Eulenburg. "Glycine transporters: essential regulators of synaptic transmission." Biochemical Society Transactions 34, no. 1 (2006): 55–58. http://dx.doi.org/10.1042/bst0340055.

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Glycine is a major inhibitory neurotransmitter in the mammalian CNS (central nervous system). Glycinergic neurotransmission is terminated by the uptake of glycine into glycinergic nerve terminals and neighbouring glial cells. This uptake process is mediated by specific Na+/Cl−-dependent GlyTs (glycine transporters), GlyT1 and GlyT2. GlyT1, in addition, is thought to regulate the concentration of glycine at excitatory synapses containing NMDARs (N-methyl-D-aspartate receptors), which require glycine as a co-agonist. We have analysed the physiological roles and regulation of GlyT1 and GlyT2 by g

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Richardson, Ben D., and David J. Rossi. "Recreational concentrations of alcohol enhance synaptic inhibition of cerebellar unipolar brush cells via pre- and postsynaptic mechanisms." Journal of Neurophysiology 118, no. 1 (2017): 267–79. http://dx.doi.org/10.1152/jn.00963.2016.

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Variation in cerebellar sensitivity to alcohol/ethanol (EtOH) is a heritable trait associated with alcohol use disorder in humans and high EtOH consumption in rodents, but the underlying mechanisms are poorly understood. A recently identified cellular substrate of cerebellar sensitivity to EtOH, the GABAergic system of cerebellar granule cells (GCs), shows divergent responses to EtOH paralleling EtOH consumption and motor impairment phenotype. Although GCs are the dominant afferent integrator in the cerebellum, such integration is shared by unipolar brush cells (UBCs) in vestibulocerebellar lo

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Cantaut-Belarif, Yasmine, Myriam Antri, Rocco Pizzarelli, et al. "Microglia control the glycinergic but not the GABAergic synapses via prostaglandin E2 in the spinal cord." Journal of Cell Biology 216, no. 9 (2017): 2979–89. http://dx.doi.org/10.1083/jcb.201607048.

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Microglia control excitatory synapses, but their role in inhibitory neurotransmission has been less well characterized. Herein, we show that microglia control the strength of glycinergic but not GABAergic synapses via modulation of the diffusion dynamics and synaptic trapping of glycine (GlyR) but not GABAA receptors. We further demonstrate that microglia regulate the activity-dependent plasticity of glycinergic synapses by tuning the GlyR diffusion trap. This microglia–synapse cross talk requires production of prostaglandin E2 by microglia, leading to the activation of neuronal EP2 receptors

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Zhang, Bo, Ozgun Gokce, W. Dylan Hale, Nils Brose, and Thomas C. Südhof. "Autism-associated neuroligin-4 mutation selectively impairs glycinergic synaptic transmission in mouse brainstem synapses." Journal of Experimental Medicine 215, no. 6 (2018): 1543–53. http://dx.doi.org/10.1084/jem.20172162.

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In human patients, loss-of-function mutations of the postsynaptic cell-adhesion molecule neuroligin-4 were repeatedly identified as monogenetic causes of autism. In mice, neuroligin-4 deletions caused autism-related behavioral impairments and subtle changes in synaptic transmission, and neuroligin-4 was found, at least in part, at glycinergic synapses. However, low expression levels precluded a comprehensive analysis of neuroligin-4 localization, and overexpression of neuroligin-4 puzzlingly impaired excitatory but not inhibitory synaptic function. As a result, the function of neuroligin-4 rem

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Yang, Kun, Tsugumi Fujita, and Eiichi Kumamoto. "Adenosine Inhibits GABAergic and Glycinergic Transmission in Adult Rat Substantia Gelatinosa Neurons." Journal of Neurophysiology 92, no. 5 (2004): 2867–77. http://dx.doi.org/10.1152/jn.00291.2004.

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The effect of adenosine on inhibitory postsynaptic currents (IPSCs) was examined in substantia gelatinosa (SG) neurons of adult rat spinal cord slices by using the whole cell patch-clamp technique. Adenosine reversibly reduced the amplitude of GABAergic and glycinergic electrically evoked IPSCs (eIPSCs) in a dose-dependent manner (EC50 = 14.5 and 19.1 μM, respectively). The A1 adenosine-receptor agonist N6-cyclopentyladenosine also reduced the eIPSCs, whereas the A1 antagonist 8-cyclopentyl-1,3-dimethylxanthine reversed the inhibition produced by adenosine. In paired-pulse experiments, the rat

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Coleman, W. L., M. J. Fischl, S. R. Weimann, and R. M. Burger. "GABAergic and glycinergic inhibition modulate monaural auditory response properties in the avian superior olivary nucleus." Journal of Neurophysiology 105, no. 5 (2011): 2405–20. http://dx.doi.org/10.1152/jn.01088.2010.

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The superior olivary nucleus (SON) is the primary source of inhibition in the avian auditory brainstem. While much is known about the role of inhibition at the SON's target nuclei, little is known about how the SON itself processes auditory information or how inhibition modulates these properties. Additionally, the synaptic physiology of inhibitory inputs within the SON has not been described. We investigated these questions using in vivo and in vitro electrophysiological techniques in combination with immunohistochemistry in the chicken, an organism for which the auditory brainstem has otherw

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Oda, Y., S. Charpier, Y. Murayama, C. Suma, and H. Korn. "Long-term potentiation of glycinergic inhibitory synaptic transmission." Journal of Neurophysiology 74, no. 3 (1995): 1056–74. http://dx.doi.org/10.1152/jn.1995.74.3.1056.

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1. Tetanizing protocols were used to test whether glycinergic inhibition undergoes long-term plasticity in vivo. For this purpose we studied the inhibition evoked disynaptically in the teleost Mauthner (M) cell by stimulation of the posterior branch of the contralateral VIIIth nerve. The advantage of this experimental design is that the inhibition, which is mediated by identified second-order commissural interneurons, is not contaminated by parallel excitation. 2. The VIIIth-nerve-evoked inhibitory postsynaptic potentials (IPSPs), which are generated at the level of the soma, are depolarizing

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