Academic literature on the topic 'Glycinergic synaptic current'
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Journal articles on the topic "Glycinergic synaptic current"
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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 (August 1, 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 pharmacological block of GABABreceptors. Glycinergic currents were comparatively much less enhanced than GABAergic currents. One possible mechanism to account for this difference is that GABAergic currents decayed so slowly that consecutive responses summated over an incrementing baseline. However, while synaptic summation appeared at ≥10-Hz stimulation, at 5 Hz strong facilitation developed with minimal summation of GABA-mediated currents. Glycinergic currents decayed so fast that summation was minimal. As [Ca2+]o is known to shape short-term synaptic changes, we examined if varying [Ca2+]o could differentially affect facilitation of GABA- or glycine-operated synapses. With 5 mM [Ca2+]o, the frequency of spontaneous GABAergic or glycinergic currents appeared much higher but GABAergic current facilitation was blocked (and replaced by depression), whereas glycinergic currents remained slightly facilitated. [Ca2+]omanipulation thus brought about distinct processes responsible for facilitation of GABAergic or glycinergic transmission. Our data therefore demonstrate an unexpectedly robust, short-term increase in the efficiency of GABAergic synapses that can become at least as effective as glycinergic synapses.
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Ghavanini, Amer A., David A. Mathers, Hee-Soo Kim, and Ernest Puil. "Distinctive Glycinergic Currents With Fast and Slow Kinetics in Thalamus." Journal of Neurophysiology 95, no. 6 (June 2006): 3438–48. http://dx.doi.org/10.1152/jn.01218.2005.
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We examined functional properties of inhibitory postsynaptic currents (IPSCs) evoked by medial lemniscal stimulation, spontaneous IPSCs (sIPSCs), and single-channel, extrasynaptic currents evoked by glycine receptor agonists or γ-aminobutyric acid (GABA) in rat ventrobasal thalamus. We identified synaptic currents by reversal at ECl and sensitivity to elimination by strychnine, GABAA antagonists, or combined application. Glycinergic IPSCs featured short (about 12 ms) and long (about 80 ms) decay time constants. These fast and slow IPSCs occurred separately with monoexponential decays, or together with biexponential decay kinetics. Glycinergic sIPSCs decayed monoexponentially with time constants, matching fast and slow IPSCs. These findings were consistent with synaptic responses generated by two populations of glycine receptors, localized under different nerve terminals. Glycine, taurine, or β-alanine applied to excised membrane patches evoked short- and long-duration current bursts. Extrasynaptic burst durations resembled fast and slow IPSC time constants. The single, intermediate time constant (about 22 ms) of GABAAergic IPSCs cotransmitted with glycinergic IPSCs approximated the burst duration of extrasynaptic GABAA channels. We noted differences between synaptic and extrasynaptic receptors. Endogenously activated glycine and GABAA receptor channels had higher Cl− permeability than that of their extrasynaptic counterparts. The β-amino acids activated long-duration bursts at extrasynaptic glycine receptors, consistent with a role in detection of ambient taurine or β-alanine. Heterogenous kinetics and permeabilities implicate molecular and functional diversity in thalamic glycine receptors. Fast, intermediate, and slow inhibitory postsynaptic potential decays, mostly attributed to cotransmission by glycinergic and GABAergic pathways, allow for discriminative modulation and integration with voltage-dependent currents in ventrobasal neurons.
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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 (October 1, 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 dorsal motor nucleus of the vagus (DMV) neurons from postnatal days 1–30, and the effects of the GABAA receptor antagonist bicuculline (1–10 μM) and the glycine receptor antagonist strychnine (1 μM) on miniature inhibitory postsynaptic current (mIPSC) properties were examined. While the baseline frequency of mIPSCs was not altered by maturation, perfusion with bicuculline either abolished mIPSCs altogether or decreased mIPSC frequency and decay constant in the majority of neurons at all time points. In contrast, while strychnine had no effect on mIPSC frequency, its actions to increase current decay time declined during postnatal maturation. These data suggest that in early postnatal development, DMV neurons receive both GABAergic and glycinergic synaptic inputs. Glycinergic neurotransmission appears to decline by the second postnatal week, and adult neurons receive principally GABAergic inhibitory inputs. Disruption of this developmental switch from GABA-glycine to purely GABAergic transmission in response to early life events may, therefore, lead to adverse consequences in vagal efferent control of visceral functions.
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TRAN, MY N., MATTHEW H. HIGGS, and PETER D. LUKASIEWICZ. "AMPA receptor kinetics limit retinal amacrine cell excitatory synaptic responses." Visual Neuroscience 16, no. 5 (September 1999): 835–42. http://dx.doi.org/10.1017/s0952523899165039.
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Amacrine cells that respond transiently to maintained illumination are thought to mediate transient inhibitory input to ganglion cells. The excitation of these transient amacrine cells is thought to be limited by inhibitory feedback to bipolar cells. We investigated the possibility that desensitizing AMPA and/or kainate (KA) receptors on amacrine cells might also limit the duration of amacrine cell excitation. To determine how these receptors might affect amacrine cell input and output, we made whole-cell recordings from amacrine and ganglion cells in the salamander retinal slice. The specific AMPA receptor antagonist GYKI-53655 blocked non-NMDA receptor-mediated amacrine cell excitatory postsynaptic currents (EPSCs) and kainate puff-elicited currents, indicating that AMPA, and not KA, receptors mediated the responses. Cyclothiazide, an agent that reduces AMPA receptor desensitization, increased the amplitude and duration of amacrine cell EPSCs. To measure the output of transient amacrine cells, we recorded glycinergic inhibitory postsynaptic currents (IPSCs) from ganglion cells, and found that these were also enhanced by cyclothiazide. Thus, prolongation of amacrine cell AMPA receptor activation enhanced amacrine cell output. Current responses elicited by puffing glycine onto ganglion cell dendrites were not affected by cyclothiazide, indicating that the enhancement of glycinergic IPSCs was not due to a direct effect on glycine receptors. These data suggest that rapid AMPA receptor desensitization and/or deactivation limits glycinergic amacrine cell excitation and the resulting inhibitory synaptic output.
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Tadros, M. A., K. E. Farrell, P. R. Schofield, A. M. Brichta, B. A. Graham, A. J. Fuglevand, and R. J. Callister. "Intrinsic and synaptic homeostatic plasticity in motoneurons from mice with glycine receptor mutations." Journal of Neurophysiology 111, no. 7 (April 1, 2014): 1487–98. http://dx.doi.org/10.1152/jn.00728.2013.
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Inhibitory synaptic inputs to hypoglossal motoneurons (HMs) are important for modulating excitability in brainstem circuits. Here we ask whether reduced inhibition, as occurs in three murine mutants with distinct naturally occurring mutations in the glycine receptor (GlyR), leads to intrinsic and/or synaptic homeostatic plasticity. Whole cell recordings were obtained from HMs in transverse brainstem slices from wild-type ( wt), spasmodic ( spd), spastic ( spa), and oscillator ( ot) mice (C57Bl/6, approximately postnatal day 21). Passive and action potential (AP) properties in spd and ot HMs were similar to wt. In contrast, spa HMs had lower input resistances, more depolarized resting membrane potentials, higher rheobase currents, smaller AP amplitudes, and slower afterhyperpolarization current decay times. The excitability of HMs, assessed by “gain” in injected current/firing-frequency plots, was similar in all strains whereas the incidence of rebound spiking was increased in spd. The difference between recruitment and derecruitment current (i.e., Δ I) for AP discharge during ramp current injection was more negative in spa and ot. GABAA miniature inhibitory postsynaptic current (mIPSC) amplitude was increased in spa and ot but not spd, suggesting diminished glycinergic drive leads to compensatory adjustments in the other major fast inhibitory synaptic transmitter system in these mutants. Overall, our data suggest long-term reduction in glycinergic drive to HMs results in changes in intrinsic and synaptic properties that are consistent with homeostatic plasticity in spa and ot but not in spd. We propose such plasticity is an attempt to stabilize HM output, which succeeds in spa but fails in ot.
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Buss, Robert R., and Pierre Drapeau. "Synaptic Drive to Motoneurons During Fictive Swimming in the Developing Zebrafish." Journal of Neurophysiology 86, no. 1 (July 1, 2001): 197–210. http://dx.doi.org/10.1152/jn.2001.86.1.197.
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The development of swimming behavior and the correlated activity patterns recorded in motoneurons during fictive swimming in paralyzed zebrafish larvae were examined and compared. Larvae were studied from when they hatch (after 2 days) and are first capable of locomotion to when they are active swimmers capable of capturing prey (after 4 days). High-speed (500 Hz) video imaging was used to make a basic behavioral characterization of swimming. At hatching and up to day 3, the larvae swam infrequently and in an undirected fashion. They displayed sustained bursts of contractions (‘burst swimming’) at an average frequency of 60–70 Hz that lasted from several seconds to a minute in duration. By day 4 the swimming had matured to a more frequent and less erratic “beat-and-glide” mode, with slower (∼35 Hz) beats of contractions for ∼200 ms alternating with glides that were twice as long, lasting from just a few cycles to several minutes overall. In whole cell current-clamp recordings, motoneurons displayed similar excitatory synaptic activity and firing patterns, corresponding to either fictive burst swimming (day 2–3) or beat-and-glide swimming (day 4). The resting potentials were similar at all stages (about −70 mV) and the motoneurons were depolarized (to about −40 mV) with generally non-overshooting action potentials during fictive swimming. The frequency of sustained inputs during fictive burst swimming and of repetitive inputs during fictive beat-and glide swimming corresponded to the behavioral contraction patterns. Fictive swimming activity patterns were eliminated by application of glutamate antagonists (kynurenic acid or 6-cyano-7-nitroquinoxalene-2,3-dione anddl-2-amino-5-phosphonovaleric acid) and were modified but maintained in the presence of the glycinergic antagonist strychnine. The corresponding synaptic currents underlying the synaptic drive to motoneurons during fictive swimming could be isolated under voltage clamp and consisted of cationic [glutamatergic postsynaptic currents (PSCs)] and anionic inputs (glycinergic PSCs). Either sustained or interrupted patterns of PSCs were observed during fictive burst or beat-and-glide swimming, respectively. During beat-and-glide swimming, a tonic inward current and rhythmic glutamatergic PSCs (∼35 Hz) were observed. In contrast, bursts of glycinergic PSCs occurred at a higher frequency, resulting in a more tonic pattern with little evidence for synchronized activity. We conclude that a rhythmic glutamatergic synaptic drive underlies swimming and that a tonic, shunting glycinergic input acts to more closely match the membrane time constant to the fast synaptic drive.
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CROOK, JOANNA D., ORIN S. PACKER, and DENNIS M. DACEY. "A synaptic signature for ON- and OFF-center parasol ganglion cells of the primate retina." Visual Neuroscience 31, no. 1 (November 27, 2013): 57–84. http://dx.doi.org/10.1017/s0952523813000461.
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AbstractIn the primate retina, parasol ganglion cells contribute to the primary visual pathway via the magnocellular division of the lateral geniculate nucleus, display ON and OFF concentric receptive field structure, nonlinear spatial summation, and high achromatic temporal–contrast sensitivity. Parasol cells may be homologous to the alpha-Y cells of nonprimate mammals where evidence suggests that N-methyl-D-aspartate (NMDA) receptor-mediated synaptic excitation as well as glycinergic disinhibition play critical roles in contrast sensitivity, acting asymmetrically in OFF- but not ON-pathways. Here, light-evoked synaptic currents were recorded in the macaque monkey retina in vitro to examine the circuitry underlying parasol cell receptive field properties. Synaptic excitation in both ON and OFF types was mediated by NMDA as well as α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate glutamate receptors. The NMDA-mediated current–voltage relationship suggested high Mg2+ affinity such that at physiological potentials, NMDA receptors contributed ∼20% of the total excitatory conductance evoked by moderate stimulus contrasts and temporal frequencies. Postsynaptic inhibition in both ON and OFF cells was dominated by a large glycinergic “crossover” conductance, with a relatively small contribution from GABAergic feedforward inhibition. However, crossover inhibition was largely rectified, greatly diminished at low stimulus contrasts, and did not contribute, via disinhibition, to contrast sensitivity. In addition, attenuation of GABAergic and glycinergic synaptic inhibition left center–surround and Y-type receptive field structure and high temporal sensitivity fundamentally intact and clearly derived from modulation of excitatory bipolar cell output. Thus, the characteristic spatial and temporal–contrast sensitivity of the primate parasol cell arises presynaptically and is governed primarily by modulation of the large AMPA/kainate receptor-mediated excitatory conductance. Moreover, the negative feedback responsible for the receptive field surround must derive from a nonGABAergic mechanism.
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Oku, Y., S. Hülsmann, W. Zhang, and D. W. Richter. "Modulation of glycinergic synaptic current kinetics by octanol in mouse hypoglossal motoneurons." Pfl�gers Archiv European Journal of Physiology 438, no. 5 (September 17, 1999): 656–64. http://dx.doi.org/10.1007/s004240051090.
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Oku, Y., S. Hülsmann, W. Zhang, and D. W. Richter. "Modulation of glycinergic synaptic current kinetics by octanol in mouse hypoglossal motoneurons." Pflügers Archiv - European Journal of Physiology 438, no. 5 (October 1999): 656–64. http://dx.doi.org/10.1007/s004249900089.
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Xie (解瑞立), Ruili, and Paul B. Manis. "Glycinergic synaptic transmission in the cochlear nucleus of mice with normal hearing and age-related hearing loss." Journal of Neurophysiology 110, no. 8 (October 15, 2013): 1848–59. http://dx.doi.org/10.1152/jn.00151.2013.
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The principal inhibitory neurotransmitter in the mammalian cochlear nucleus (CN) is glycine. During age-related hearing loss (AHL), glycinergic inhibition becomes weaker in CN. However, it is unclear what aspects of glycinergic transmission are responsible for weaker inhibition with AHL. We examined glycinergic transmission onto bushy cells of the anteroventral CN in normal-hearing CBA/CaJ mice and in DBA/2J mice, a strain that exhibits an early onset AHL. Glycinergic synaptic transmission was examined in brain slices of mice at 10–15 postnatal days old, 20–35 days old, and at 6–7 mo old. Spontaneous inhibitory postsynaptic current (sIPSC) event frequency and amplitude were the same among all three ages in both strains of mice. However, the amplitudes of IPSCs evoked (eIPSC) from stimulating the dorsal CN were smaller, and the failure rate was higher, with increasing age due to decreased quantal content in both mouse strains, independent of hearing status. The coefficient of variation of the eIPSC amplitude also increased with age. The decay time constant (τ) of sIPSCs and eIPSCs were constant in CBA/CaJ mice at all ages, but were significantly slower in DBA/2J mice at postnatal days 20–35, following the onset of AHL, and not at earlier or later ages. Our results suggest that glycinergic inhibition at the synapses onto bushy cells becomes weaker and less reliable with age through changes in release. However, the hearing loss in DBA/2J mice is accompanied by a transiently enhanced inhibition, which could disrupt the balance of excitation and inhibition.
Dissertations / Theses on the topic "Glycinergic synaptic current"
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Rančić, Vladimir. "Characterization of synaptic circuits changes in ventral horn of embrionic spinal slices cultures from SOD1 G93A mice." Doctoral thesis, Università degli studi di Trieste, 2011. http://hdl.handle.net/10077/4598.
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2009/2010Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease characterized by loss of motoneurons. The discovery of mutations in the gene for the cytosolic Cu/Zn superoxide dismutase in a small proportion of familiar ALS patients led to an animal model in which the human mutant SOD1 is overexpressed in mice (G93A). For this study, we employed the long term spinal cord organotypic cultures developed from G93A embryonic mice and their wild type (WT) littermates, starting from the recent findings emerged from a study by Avossa et al. (2006). These authors reported that G93A organotypic spinal cultures exhibited increased vulnerability to AMPA glutamate receptormediated excitotoxic stress, prior to clear disease appearance, besides showing a significantly increased ratio between inhibitory and excitatory synapses, although they did not express evident morphological differences, when compared to WT ones (Avossa et al., 2006). The primary objective of this study was to investigate this early ALS stage to understand how functional changes can predate morphological alterations. To that aim we monitored spontaneous synaptic activity via patch clamping interneurons both in WT and G93A spinal cultures after 7, 14 and 21 days of in vitro (DIV) growth. At 7 DIV, when synchronous episodes of activity are normally detected in cultured spinal circuits, G93A slices displayed bursting with a higher probability (83%) when compared to controls (54%). Between 14 and 21 DIV, when bursting activity disappear, both in G93A and WT slices, pharmacological dissection of glutamate, GABA and glycine mediated post synaptic currents (PSCs), showed, in G93A, a significant reduction in GABAergic PSCs and mPSCs in respect to WT. Upon pharmacological removal of the GABAergic component, fast glycinergic events were unmasked and these events displayed a similar frequency in both culture groups. Along with in vitro growth, we detected a progressive reduction in the decay time constant of glycinergic PSCs, such process was significantly faster in G93A. Thus, a shift in dynamic communication within spinal networks might be involved in ALS progression.
XXIII Ciclo
1980