Inhibitory Control at a Synaptic Relay

Awatramani, Gautam B.; Tureček, Rostislav; Trussell, Laurence O.

doi:10.1523/jneurosci.5144-03.2004

Cited by 76 publications

(87 citation statements)

References 52 publications

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“…Blocking GABAergic or glycinergic inhibition can eliminate duration tuning, suggesting that the neural code for sound duration is the result of convergence of excitatory and inhibitory inputs (Casseday et al, 2000). The matching of excitatory transmission in the calyx of Held by a powerful, precision glycinergic inhibitory system suggests that the relay function of the medial nucleus of the trapezoid body of rats may be rapidly modified during sound localization (Awatramani et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Glycine Receptors in CNS Neurons as a Target for Nonretrograde Action of Cannabinoids

Lozovaya

Yatsenko²,

Beketov³

et al. 2005

J. Neurosci.

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At many central synapses, endocannabinoids released by postsynaptic cells act retrogradely on presynaptic G-protein-coupled cannabinoid receptors to inhibit neurotransmitter release. Here, we demonstrate that cannabinoids may directly affect the functioning of inhibitory glycine receptor (GlyR) channels. In isolated hippocampal pyramidal and Purkinje cerebellar neurons, endogenous cannabinoids anandamide and 2-arachidonylglycerol, applied at physiological concentrations, inhibited the amplitude and altered the kinetics of rise time, desensitization, and deactivation of the glycine-activated current (I Gly ) in a concentration-dependent manner. These effects of cannabinoids were observed in the presence of cannabinoid CB1/CB3, vanilloid receptor 1 antagonists, and the G-protein inhibitor GDP␤S, suggesting a direct action of cannabinoids on GlyRs. The effect of cannabinoids on I Gly desensitization was strongly voltage dependent. We also demonstrate that, in the presence of a GABA A receptor antagonist, GlyRs may contribute to the generation of seizure-like activity induced by short bursts (seven stimuli) of high-frequency stimulation of inputs to hippocampal CA1 region, because this activity was diminished by selective GlyR antagonists (strychnine and ginkgolides B and J). The GlyR-mediated rhythmic activity was also reduced by cannabinoids (anandamide) in the presence of a CB1 receptor antagonist. These results suggest that the direct inhibition of GlyRs by endocannabinoids can modulate the hippocampal network activity.

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Section: Discussionmentioning

confidence: 99%

Glycine Receptors in CNS Neurons as a Target for Nonretrograde Action of Cannabinoids

Lozovaya

Yatsenko²,

Beketov³

et al. 2005

J. Neurosci.

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“…An Iso-Flex stimulator driven by a Master 8 pulse generator (A.M.P.I., Jerusalem, Israel) was used to deliver step pulses (100 s, Ͻ15 V DC). EPSCs were recorded in normal aCSF containing D-APV (50 M) and MK-801 ((ϩ)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate; 5 M) to isolate AMPA receptor currents and strychnine (0.5 M) to eliminate inhibitory transmission present, especially in older MNTB (Awatramani et al, 2004). Recordings of miniature EPSCs (mEPSCs) also contained tetrodotoxin (TTX; 1 mM) in some cases, although results were identical with or without TTX.…”

Section: Methodsmentioning

confidence: 99%

Physiological Temperatures Reduce the Rate of Vesicle Pool Depletion and Short-Term Depression via an Acceleration of Vesicle Recruitment

2006

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The timing and strength of synaptic transmission is profoundly dependent on temperature. However, the temperature dependence of the multiple mechanisms that contribute to short-term synaptic plasticity is poorly understood. Here, we use voltage-clamp recordings to quantify the temperature dependence of exocytosis at the calyx of Held synapse. EPSC and miniature EPSC amplitudes were larger at physiological temperature, but quantal content during low-frequency (0.05 Hz) stimulation was constant after temperature jumps from 22-24°C to 35-37°C. The initial degree of EPSC depression during 100 Hz stimuli trains was unchanged with temperature, as were estimates of release probability and vesicle pool size. In contrast, physiological temperatures dramatically relieved depression measured after 40 stimuli at 100 Hz by increasing twofold the rate of recovery from depression. Presynaptic calyx recordings revealed that physiological temperature increased capacitance jumps resulting from 0.5 and 1 ms depolarizations by increasing Ca 2ϩ influx. When Ca 2ϩ entry was equalized at the two temperatures, exocytosis exhibited little temperature dependence for brief depolarizations. However, in response to longer depolarizations, raising temperature increased a slow phase of exocytosis, without affecting overall Ca 2ϩ entry or the size of the readily releasable pool of vesicles. Higher temperatures also increased the rate of presynaptic Ca 2ϩ current inactivation; nevertheless, the degree of steady-state EPSC depression was greatly reduced. Our results thus suggest that changes in steady-state EPSCs during stimulus trains at physiological temperature reflect larger quantal amplitudes and faster refilling of synaptic vesicle pools, leading to reduced short-term depression during prolonged high-frequency firing.

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“…112: 2901-2915. First published September 3, 2014 doi:10.1152/jn.00864.2013 preparations (Awatramani et al 2004). The results suggest that inhibitory inputs to MNTB retain substantial synaptic amplitudes even after being challenged with long stimulus trains consisting of thousands of pulses.…”

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confidence: 99%

“…Moreover, MNTB neurons themselves receive synaptic inhibition (Albrecht et al 2014;Awatramani et al 2004;Green and Sanes 2005;Smith et al 1998;Thompson and Schofield 2000), which modifies firing patterns of MNTB neurons (Green and Sanes 2005; KoppScheinpflug et al 2008;Tolnai et al 2008).…”

mentioning

confidence: 99%

“…Physiological properties of excitatory inputs to MNTB neurons change substantially when this chronic activity is absent from slice preparations (Hermann et al 2007(Hermann et al , 2009). The main question we addressed in this study was how the properties of inhibitory postsynaptic current (IPSC) amplitudes would change when investigated under conditions of chronic activity and high firing rates compared with their properties in silent brain slice preparations (Awatramani et al 2004). The results suggest that inhibitory inputs to MNTB retain substantial synaptic amplitudes even after being challenged with long stimulus trains consisting of thousands of pulses.…”

mentioning

confidence: 99%

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Glycinergic inhibition to the medial nucleus of the trapezoid body shows prominent facilitation and can sustain high levels of ongoing activity

Mayer

Albrecht

Dondzillo

et al. 2014

Journal of Neurophysiology

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tion to the medial nucleus of the trapezoid body shows prominent facilitation and can sustain high levels of ongoing activity. J Neurophysiol 112: 2901-2915. First published September 3, 2014 doi:10.1152/jn.00864.2013.-Neurons in the medial nucleus of the trapezoid body (MNTB) are well known for their prominent excitatory inputs, mediated by the calyx of Held. Less attention has been paid to the prominent inhibitory inputs that MNTB neurons also receive. Because of their auditory nature, both excitatory and inhibitory synapses are highly active in vivo. These high levels of activity are known to reduce excitatory synaptic currents considerably, such that in vivo synaptic currents produced by the calyx are smaller than typically measured in standard brain slice experiments. The goal of this study was to investigate the properties of the inhibitory inputs in the Mongolian gerbil (Meriones unguiculatus) under activity levels that correspond to those in the intact brain to facilitate a direct comparison between the two inputs. Our results suggest that inhibitory inputs to MNTB are largely mediated by a fast and phasic glycinergic component, and to a lesser degree by a GABAergic component. The glycinergic component can sustain prolonged high levels of activity. Even when challenged with stimulus patterns consisting of thousands of stimuli over tens of minutes, glycinergic inputs to MNTB maintain large conductances and fast decays and even facilitate substantially when the stimulation frequency is increased. The inhibition is mediated by a relatively small number of independent input fibers. The data presented here suggest that inhibitory inputs to MNTB sustain high levels of activity and need to be considered for a full understanding of mechanisms underlying processing of auditory information in MNTB. auditory brain stem; inhibition; medial nucleus of the trapezoid body; calyx of Held; short-term plasticity SYNAPTIC TRANSMISSION in the medial nucleus of the trapezoid body (MNTB) has been studied extensively over the last years. Principal neurons in the MNTB receive neural excitation via a giant synapse, the calyx of Held (Borst et al. 1995;Borst and Soria van Hoeve 2012;Forsythe 1994;Held 1892Held , 1893Tolbert et al. 1982). Synaptic currents produced by the calyx are large and fast, and both the calyx and the postsynaptic neuron have a number of adaptations suited to transmit action potentials with very high temporal fidelity (Guinan and Li 1990;Kochubey et al. 2009;Taschenberger and von Gersdorff 2000). Besides temporal precision, it has been argued that one reason for the large excitatory signals is that the calyx of Held/MNTB system is a fail-safe relay station that simply converts glutamatergic excitation into glycinergic inhibition without any significant spike train transformation (Borst and Soria van Hoeve 2012;Crins et al. 2011;McLaughlin et al. 2008;Smith et al. 1998;Taschenberger and von Gersdorff 2000). The sign inversion is needed because neural inhibition is required in the sound localization process i...

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Inhibitory Control at a Synaptic Relay

Cited by 76 publications

References 52 publications

Glycine Receptors in CNS Neurons as a Target for Nonretrograde Action of Cannabinoids

Glycine Receptors in CNS Neurons as a Target for Nonretrograde Action of Cannabinoids

Physiological Temperatures Reduce the Rate of Vesicle Pool Depletion and Short-Term Depression via an Acceleration of Vesicle Recruitment

Glycinergic inhibition to the medial nucleus of the trapezoid body shows prominent facilitation and can sustain high levels of ongoing activity

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