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Michael H. Chase - One of the best experts on this subject based on the ideXlab platform.
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0066 Glycinergic Postsynaptic Inhibition is Responsible for the Suppression of Hypoglossal Motoneuron Activity During Naturally-Occurring REM Sleep
Sleep, 2020Co-Authors: C Tobin, Simon J Fung, Michael H. ChaseAbstract:Abstract Introduction The present study was undertaken to explore the role of glycinergic Postsynaptic Inhibition and monoaminergic disfacilitation (a withdrawal of excitatory noradrenergic and serotonergic inputs) in the control of hypoglossal motoneuron activity during REM sleep. Accordingly, glycinergic, noradrenergic and serotonergic antagonists were microinjected into the hypoglossal nucleus, and their effects on the hypoglossal nerve activity during REM sleep were examined in chronically-instrumented, unanesthetized cats. Methods Adults cats were prepared for monitoring behavioral states of sleep and wakefulness, and for extracellular recordings from hypoglossal nerve. Strychnine (a glycinergic antagonist) and a mixture of prazosin (a noradrenergic antagonist) and methysergide (a serotonergic antagonist) were microinjected, separately, into the hypoglossal nucleus during naturally-occurring states of sleep and wakefulness. Results During REM sleep, compared to non-REM sleep, the hypoglossal nerve activity decreased by 17.4±1.5% (n=17) in the control recordings (prior to the injection of strychnine). Following the microinjection of strychnine, there was only a mean decrease of 7.2±1.2% (n=12) in the nerve activity during REM sleep versus NREM sleep. The strychnine effect was statistically significant compared to control (p<0.001; unpaired t-test), which indicates that strychnine blocks REM sleep-related suppression of hypoglossal nerve activity. In contrast, the microinjection of prazosin and methysergide did not significantly reduce the hypoglossal nerve activity during REM sleep (control: 15.9±2.3, n=9 vs. prazosin+methysergide: 12.6±1.4%, n=10, p=0.229, unpaired t-test). Conclusion The present results demonstrate that the microapplication of strychnine, but not prazosin and methysergide, into the hypoglossal nucleus significantly reduces the suppression of the hypoglossal nerve activity during naturally-occurring REM sleep. We therefore suggest that glycinergic Postsynaptic Inhibition is primarily responsible for the suppression of hypoglossal motoneuron activity during REM sleep. Support 5R01NS094062
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Postsynaptic Inhibition of hypoglossal motoneurons produces atonia of the genioglossal muscle during rapid eye movement sleep
Sleep, 2015Co-Authors: Simon J Fung, Michael H. ChaseAbstract:Study Objectives: Hypoglossal motoneurons were recorded intracellularly to determine whether Postsynaptic Inhibition or disfacilitation was responsible for atonia of the lingual muscles during rapid eye movement (REM) sleep. Design: Intracellular records were obtained of the action potentials and subthreshold membrane potential activity of antidromically identified hypoglossal motoneurons in cats during wakefulness, nonrapid eye movement (NREM) sleep, and REM sleep. A cuff electrode was placed around the hypoglossal nerve to antidromically activate hypoglossal motoneurons. The state-dependent changes in membrane potential, spontaneous discharge, Postsynaptic potentials, and rheobase of hypoglossal motoneurons were determined. Analyses and Results: During quiet wakefulness and NREM sleep, hypoglossal motoneurons exhibited spontaneous repetitive discharge. In the transition from NREM sleep to REM sleep, repetitive discharge ceased and the membrane potential began to hyperpolarize; maximal hyperpolarization (10.5 mV) persisted throughout REM sleep. During REM sleep there was a significant increase in rheobase, which was accompanied by barrages of large-amplitude inhibitory Postsynaptic potentials (IPSPs), which were reversed following the intracellular injection of chloride ions. The latter result indicates that they were mediated by glycine; IPSPs were not present during wakefulness or NREM sleep. Conclusions: We conclude that hypoglossal motoneurons are Postsynaptically inhibited during naturally occurring REM sleep; no evidence of disfacilitation was observed. The data also indicate that glycine receptor-mediated Postsynaptic Inhibition of hypoglossal motoneurons is crucial in promoting atonia of the lingual muscles during REM sleep.
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Postsynaptic Inhibition of Hypoglossal Motoneurons Produces Atonia of the Genioglossal Muscle During Rapid Eye Movement Sleep
Sleep, 2015Co-Authors: Simon J Fung, Michael H. ChaseAbstract:Study Objectives: Hypoglossal motoneurons were recorded intracellularly to determine whether Postsynaptic Inhibition or disfacilitation was responsible for atonia of the lingual muscles during rapid eye movement (REM) sleep. Design: Intracellular records were obtained of the action potentials and subthreshold membrane potential activity of antidromically identified hypoglossal motoneurons in cats during wakefulness, nonrapid eye movement (NREM) sleep, and REM sleep. A cuff electrode was placed around the hypoglossal nerve to antidromically activate hypoglossal motoneurons. The state-dependent changes in membrane potential, spontaneous discharge, Postsynaptic potentials, and rheobase of hypoglossal motoneurons were determined. Analyses and Results: During quiet wakefulness and NREM sleep, hypoglossal motoneurons exhibited spontaneous repetitive discharge. In the transition from NREM sleep to REM sleep, repetitive discharge ceased and the membrane potential began to hyperpolarize; maximal hyperpolarization (10.5 mV) persisted throughout REM sleep. During REM sleep there was a significant increase in rheobase, which was accompanied by barrages of large-amplitude inhibitory Postsynaptic potentials (IPSPs), which were reversed following the intracellular injection of chloride ions. The latter result indicates that they were mediated by glycine; IPSPs were not present during wakefulness or NREM sleep. Conclusions: We conclude that hypoglossal motoneurons are Postsynaptically inhibited during naturally occurring REM sleep; no evidence of disfacilitation was observed. The data also indicate that glycine receptor-mediated Postsynaptic Inhibition of hypoglossal motoneurons is crucial in promoting atonia of the lingual muscles during REM sleep.
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Confirmation of the consensus that glycinergic Postsynaptic Inhibition is responsible for the atonia of REM sleep.
Sleep, 2008Co-Authors: Michael H. ChaseAbstract:An overwhelmingly coherent, integrated body of data developed by independent laboratories, over many decades, using intracellular recording in conjunction with the juxtacellular microiontophoretic ejection of neurotransmitters and antagonists, demonstrates conclusively that Postsynaptic Inhibition, mediated by glycine, is the critical and sufficient process that completely accounts for the suppression of motoneuron discharge during the tonic and phasic periods of REM sleep. These studies, many of which were conducted in intact, naturally sleeping, adult animals, eliminate potential interpretive complications that arise using reduced, in vitro slice or even intact in vivo preparations; they also provide for levels of resolutions that are not possible with microdialysis. On the other hand, when infusing a cocktail of substances for two to four hours into the trigeminal motor pool and adjacent regions, it is to be expected that uninterpretable and nonphysiological results would be obtained, especially when thousands of receptors on thousands of cells that are exclusively responsible for promoting waking-related functions of trigeminal motoneurons are activated. Because receptors in such a large region were indiscriminately activated by substances that Brooks and Peever dialyzed, it is clearly impossible to conclude that any change in EMG activity was due only to the activation of receptors on alpha motoneurons that are involved in state-dependent processes. In addition, because the results that Brooks and Peever obtained cannot be attributed to any specific class of receptors, synaptic process, or cell type, it is not possible to compare their findings with data obtained from intracellular studies. The preceding notwithstanding, the technical execution of their experiments was of an extremely high quality. Given this obvious strength of Brooks and Peever, it is unfortunate that they did not utilize a technique that would have allowed them to obtain meaningful data, such as intracellular recording. In point of fact, the generation of a preparation in which it is possible to record intracellularly and eject substances juxtacellularly during naturally occurring states of sleep and wakefulness was developed, over a period of two years, specifically to avoid the problems that are inherent in the microdialysis technique that Brooks and Peever employed. In conclusion, during wakefulness, numerous receptors on a great many neuronal elements in and in the vicinity of the trigeminal motor nucleus are normally activated in highly regulated sequences depending upon the specific behavior that is being performed, such as vocalization, biting, chewing, swallowing, etc. On the other hand, during REM sleep, only receptors on alpha motoneurons in the trigeminal motor nucleus, which are involved in state-dependent control processes, are excited. These latter receptors have been identified as glycinergic and have been shown to be activated, monosynaptically, by projections from the region of the nucleus reticularis gigantocellularis. Therefore, there is no justification for Brooks and Peever to claim that an unknown “biochemical substrate” is responsible for atonia during REM sleep, nor do they provide any data or reason not to continue to believe in the veracity of their initial statement, reflecting the consensus that “glycinergic Inhibition of somatic motoneurons is responsible for loss of postural muscle tone in REM sleep.”1
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Dorsal spinocerebellar tract neurons are not subjected to Postsynaptic Inhibition during carbachol-induced motor Inhibition.
Journal of Neurophysiology, 1997Co-Authors: Jack Yamuy, Rong-huan Liu, Francisco R. Morales, Michael H. ChaseAbstract:Xi, Ming-Chu, Jack Yamuy, Rong-Huan Liu, Francisco R. Morales, and Michael H. Chase. Dorsal spinocerebellar tract neurons are not subjected to Postsynaptic Inhibition during carbachol-induced motor Inhibition. J. Neurophysiol. 78: 137–144, 1997. Dorsal spinocerebellar tract (DSCT) neurons in Clarke's column in the lumbar spinal cord of cats anesthetized with α-chloralose were recorded intracellularly. The membrane potential activity and electrophysiological properties of these neurons were examined before and during the state of active-sleep-like motor Inhibition induced by the injection of carbachol into the nucleus pontis oralis. The synaptic activity of DSCT neurons during carbachol-induced motor Inhibition did not change compared with that during control conditions. In particular, there was an absence of inhibitory Postsynaptic potentials (IPSPs) in high-gain recordings from DSCT neurons and the resting membrane potential of DSCT neurons was not significantly hyperpolarized during carbachol-induced motor Inhibition. The mean amplitude of both monosynaptic excitatory Postsynaptic potentials and disynaptic IPSPs evoked in DSCT neurons following stimulation of group I muscle afferents after the injection of carbachol was similar to that evoked before the injection of carbachol. There were no significant changes in the mean input resistance and membrane time constant of DSCT neurons during carbachol-induced motor Inhibition. We conclude that, in contrast to lumbar motoneurons, DSCT neurons in Clarke's column are not Postsynaptically inhibited during carbachol-induced motor Inhibition. Therefore the population of spinal cord Ib interneurons that inhibit both DSCT neurons and lumbar motoneurons is not likely to be the interneurons that are responsible for the Postsynaptic Inhibition of motoneurons that occurs during carbachol-induced motor Inhibition. The present findings also indicate that transmission through the DSCT is not modulated by Postsynaptic Inhibition at the level of DSCT neurons during carbachol-induced motor Inhibition.
Peter D Lukasiewicz - One of the best experts on this subject based on the ideXlab platform.
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distinct ionotropic gaba receptors mediate presynaptic and Postsynaptic Inhibition in retinal bipolar cells
The Journal of Neuroscience, 2000Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D LukasiewiczAbstract:Ionotropic GABA receptors can mediate presynaptic and Postsynaptic Inhibition. We assessed the contributions of GABAA and GABAC receptors to Inhibition at the dendrites and axon terminals of ferret retinal bipolar cells by recording currents evoked by focal application of GABA in the retinal slice. Currents elicited at the dendrites were mediated predominantly by GABAA receptors, whereas responses evoked at the terminals had GABAA and GABAC components. The ratio of GABAC to GABAA(GABAC:GABAA) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABAC:GABAA could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABAC:GABAA was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABAA β2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABAC ρ subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABAA receptors mediate GABAergic Inhibition on bipolar cell dendrites in the OPL, that GABAA and GABACreceptors mediate Inhibition on axon terminals in the IPL, and that the GABAC:GABAA on the terminals may tune the response characteristics of the bipolar cell.
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Distinct Ionotropic GABA Receptors Mediate Presynaptic and Postsynaptic Inhibition in Retinal Bipolar Cells
The Journal of Neuroscience, 2000Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D LukasiewiczAbstract:Ionotropic GABA receptors can mediate presynaptic and Postsynaptic Inhibition. We assessed the contributions of GABA(A) and GABA(C) receptors to Inhibition at the dendrites and axon terminals of ferret retinal bipolar cells by recording currents evoked by focal application of GABA in the retinal slice. Currents elicited at the dendrites were mediated predominantly by GABA(A) receptors, whereas responses evoked at the terminals had GABA(A) and GABA(C) components. The ratio of GABA(C) to GABA(A) (GABA(C):GABA(A)) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABA(C):GABA(A) could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABA(C):GABA(A) was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABA(A) beta2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABA(C) rho subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABA(A) receptors mediate GABAergic Inhibition on bipolar cell dendrites in the OPL, that GABA(A) and GABA(C) receptors mediate Inhibition on axon terminals in the IPL, and that the GABA(C):GABA(A) on the terminals may tune the response characteristics of the bipolar cell.
Colleen R Shields - One of the best experts on this subject based on the ideXlab platform.
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distinct ionotropic gaba receptors mediate presynaptic and Postsynaptic Inhibition in retinal bipolar cells
The Journal of Neuroscience, 2000Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D LukasiewiczAbstract:Ionotropic GABA receptors can mediate presynaptic and Postsynaptic Inhibition. We assessed the contributions of GABAA and GABAC receptors to Inhibition at the dendrites and axon terminals of ferret retinal bipolar cells by recording currents evoked by focal application of GABA in the retinal slice. Currents elicited at the dendrites were mediated predominantly by GABAA receptors, whereas responses evoked at the terminals had GABAA and GABAC components. The ratio of GABAC to GABAA(GABAC:GABAA) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABAC:GABAA could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABAC:GABAA was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABAA β2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABAC ρ subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABAA receptors mediate GABAergic Inhibition on bipolar cell dendrites in the OPL, that GABAA and GABACreceptors mediate Inhibition on axon terminals in the IPL, and that the GABAC:GABAA on the terminals may tune the response characteristics of the bipolar cell.
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Distinct Ionotropic GABA Receptors Mediate Presynaptic and Postsynaptic Inhibition in Retinal Bipolar Cells
The Journal of Neuroscience, 2000Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D LukasiewiczAbstract:Ionotropic GABA receptors can mediate presynaptic and Postsynaptic Inhibition. We assessed the contributions of GABA(A) and GABA(C) receptors to Inhibition at the dendrites and axon terminals of ferret retinal bipolar cells by recording currents evoked by focal application of GABA in the retinal slice. Currents elicited at the dendrites were mediated predominantly by GABA(A) receptors, whereas responses evoked at the terminals had GABA(A) and GABA(C) components. The ratio of GABA(C) to GABA(A) (GABA(C):GABA(A)) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABA(C):GABA(A) could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABA(C):GABA(A) was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABA(A) beta2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABA(C) rho subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABA(A) receptors mediate GABAergic Inhibition on bipolar cell dendrites in the OPL, that GABA(A) and GABA(C) receptors mediate Inhibition on axon terminals in the IPL, and that the GABA(C):GABA(A) on the terminals may tune the response characteristics of the bipolar cell.
Simon J Fung - One of the best experts on this subject based on the ideXlab platform.
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0066 Glycinergic Postsynaptic Inhibition is Responsible for the Suppression of Hypoglossal Motoneuron Activity During Naturally-Occurring REM Sleep
Sleep, 2020Co-Authors: C Tobin, Simon J Fung, Michael H. ChaseAbstract:Abstract Introduction The present study was undertaken to explore the role of glycinergic Postsynaptic Inhibition and monoaminergic disfacilitation (a withdrawal of excitatory noradrenergic and serotonergic inputs) in the control of hypoglossal motoneuron activity during REM sleep. Accordingly, glycinergic, noradrenergic and serotonergic antagonists were microinjected into the hypoglossal nucleus, and their effects on the hypoglossal nerve activity during REM sleep were examined in chronically-instrumented, unanesthetized cats. Methods Adults cats were prepared for monitoring behavioral states of sleep and wakefulness, and for extracellular recordings from hypoglossal nerve. Strychnine (a glycinergic antagonist) and a mixture of prazosin (a noradrenergic antagonist) and methysergide (a serotonergic antagonist) were microinjected, separately, into the hypoglossal nucleus during naturally-occurring states of sleep and wakefulness. Results During REM sleep, compared to non-REM sleep, the hypoglossal nerve activity decreased by 17.4±1.5% (n=17) in the control recordings (prior to the injection of strychnine). Following the microinjection of strychnine, there was only a mean decrease of 7.2±1.2% (n=12) in the nerve activity during REM sleep versus NREM sleep. The strychnine effect was statistically significant compared to control (p<0.001; unpaired t-test), which indicates that strychnine blocks REM sleep-related suppression of hypoglossal nerve activity. In contrast, the microinjection of prazosin and methysergide did not significantly reduce the hypoglossal nerve activity during REM sleep (control: 15.9±2.3, n=9 vs. prazosin+methysergide: 12.6±1.4%, n=10, p=0.229, unpaired t-test). Conclusion The present results demonstrate that the microapplication of strychnine, but not prazosin and methysergide, into the hypoglossal nucleus significantly reduces the suppression of the hypoglossal nerve activity during naturally-occurring REM sleep. We therefore suggest that glycinergic Postsynaptic Inhibition is primarily responsible for the suppression of hypoglossal motoneuron activity during REM sleep. Support 5R01NS094062
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Postsynaptic Inhibition of hypoglossal motoneurons produces atonia of the genioglossal muscle during rapid eye movement sleep
Sleep, 2015Co-Authors: Simon J Fung, Michael H. ChaseAbstract:Study Objectives: Hypoglossal motoneurons were recorded intracellularly to determine whether Postsynaptic Inhibition or disfacilitation was responsible for atonia of the lingual muscles during rapid eye movement (REM) sleep. Design: Intracellular records were obtained of the action potentials and subthreshold membrane potential activity of antidromically identified hypoglossal motoneurons in cats during wakefulness, nonrapid eye movement (NREM) sleep, and REM sleep. A cuff electrode was placed around the hypoglossal nerve to antidromically activate hypoglossal motoneurons. The state-dependent changes in membrane potential, spontaneous discharge, Postsynaptic potentials, and rheobase of hypoglossal motoneurons were determined. Analyses and Results: During quiet wakefulness and NREM sleep, hypoglossal motoneurons exhibited spontaneous repetitive discharge. In the transition from NREM sleep to REM sleep, repetitive discharge ceased and the membrane potential began to hyperpolarize; maximal hyperpolarization (10.5 mV) persisted throughout REM sleep. During REM sleep there was a significant increase in rheobase, which was accompanied by barrages of large-amplitude inhibitory Postsynaptic potentials (IPSPs), which were reversed following the intracellular injection of chloride ions. The latter result indicates that they were mediated by glycine; IPSPs were not present during wakefulness or NREM sleep. Conclusions: We conclude that hypoglossal motoneurons are Postsynaptically inhibited during naturally occurring REM sleep; no evidence of disfacilitation was observed. The data also indicate that glycine receptor-mediated Postsynaptic Inhibition of hypoglossal motoneurons is crucial in promoting atonia of the lingual muscles during REM sleep.
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Postsynaptic Inhibition of Hypoglossal Motoneurons Produces Atonia of the Genioglossal Muscle During Rapid Eye Movement Sleep
Sleep, 2015Co-Authors: Simon J Fung, Michael H. ChaseAbstract:Study Objectives: Hypoglossal motoneurons were recorded intracellularly to determine whether Postsynaptic Inhibition or disfacilitation was responsible for atonia of the lingual muscles during rapid eye movement (REM) sleep. Design: Intracellular records were obtained of the action potentials and subthreshold membrane potential activity of antidromically identified hypoglossal motoneurons in cats during wakefulness, nonrapid eye movement (NREM) sleep, and REM sleep. A cuff electrode was placed around the hypoglossal nerve to antidromically activate hypoglossal motoneurons. The state-dependent changes in membrane potential, spontaneous discharge, Postsynaptic potentials, and rheobase of hypoglossal motoneurons were determined. Analyses and Results: During quiet wakefulness and NREM sleep, hypoglossal motoneurons exhibited spontaneous repetitive discharge. In the transition from NREM sleep to REM sleep, repetitive discharge ceased and the membrane potential began to hyperpolarize; maximal hyperpolarization (10.5 mV) persisted throughout REM sleep. During REM sleep there was a significant increase in rheobase, which was accompanied by barrages of large-amplitude inhibitory Postsynaptic potentials (IPSPs), which were reversed following the intracellular injection of chloride ions. The latter result indicates that they were mediated by glycine; IPSPs were not present during wakefulness or NREM sleep. Conclusions: We conclude that hypoglossal motoneurons are Postsynaptically inhibited during naturally occurring REM sleep; no evidence of disfacilitation was observed. The data also indicate that glycine receptor-mediated Postsynaptic Inhibition of hypoglossal motoneurons is crucial in promoting atonia of the lingual muscles during REM sleep.
My N Tran - One of the best experts on this subject based on the ideXlab platform.
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distinct ionotropic gaba receptors mediate presynaptic and Postsynaptic Inhibition in retinal bipolar cells
The Journal of Neuroscience, 2000Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D LukasiewiczAbstract:Ionotropic GABA receptors can mediate presynaptic and Postsynaptic Inhibition. We assessed the contributions of GABAA and GABAC receptors to Inhibition at the dendrites and axon terminals of ferret retinal bipolar cells by recording currents evoked by focal application of GABA in the retinal slice. Currents elicited at the dendrites were mediated predominantly by GABAA receptors, whereas responses evoked at the terminals had GABAA and GABAC components. The ratio of GABAC to GABAA(GABAC:GABAA) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABAC:GABAA could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABAC:GABAA was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABAA β2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABAC ρ subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABAA receptors mediate GABAergic Inhibition on bipolar cell dendrites in the OPL, that GABAA and GABACreceptors mediate Inhibition on axon terminals in the IPL, and that the GABAC:GABAA on the terminals may tune the response characteristics of the bipolar cell.
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Distinct Ionotropic GABA Receptors Mediate Presynaptic and Postsynaptic Inhibition in Retinal Bipolar Cells
The Journal of Neuroscience, 2000Co-Authors: Colleen R Shields, My N Tran, Rachel O L Wong, Peter D LukasiewiczAbstract:Ionotropic GABA receptors can mediate presynaptic and Postsynaptic Inhibition. We assessed the contributions of GABA(A) and GABA(C) receptors to Inhibition at the dendrites and axon terminals of ferret retinal bipolar cells by recording currents evoked by focal application of GABA in the retinal slice. Currents elicited at the dendrites were mediated predominantly by GABA(A) receptors, whereas responses evoked at the terminals had GABA(A) and GABA(C) components. The ratio of GABA(C) to GABA(A) (GABA(C):GABA(A)) was highest in rod bipolar cell terminals and variable among cone bipolars, but generally was lower in OFF than in ON classes. Our results also suggest that the GABA(C):GABA(A) could influence the time course of responses. Currents evoked at the terminals decayed slowly in cell types for which the GABA(C):GABA(A) was high, but decayed relatively rapidly in cells for which this ratio was low. Immunohistochemical studies corroborated our physiological results. GABA(A) beta2/3 subunit immunoreactivity was intense in the outer and inner plexiform layers (OPL and IPL, respectively). GABA(C) rho subunit labeling was weak in the OPL but strong in the IPL in which puncta colocalized with terminals of rod bipolars immunoreactive for protein kinase C and of cone bipolars immunoreactive for calbindin or recoverin. These data demonstrate that GABA(A) receptors mediate GABAergic Inhibition on bipolar cell dendrites in the OPL, that GABA(A) and GABA(C) receptors mediate Inhibition on axon terminals in the IPL, and that the GABA(C):GABA(A) on the terminals may tune the response characteristics of the bipolar cell.