GABAB receptors presynaptically modulate excitatory synaptic transmission in the rat supraoptic nucleus in vitro

Kombian, Samuel B.; Zidichouski, Jeffrey A.; Pittman, Quentin J.

doi:10.1152/jn.1996.76.2.1166

Cited by 77 publications

(65 citation statements)

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“…To test whether the glutamate release probability was an important determinant for the induction of burst pairing depression, we used an independent method to lower probability of release at glutamate synapses. We (Kuzmiski et al, 2009) and others (Kombian et al, 1996;Kolaj et al, 2000) have shown that GABA B receptors are powerful inhibitors of glutamate release at synapses onto MNCs. Consequently, we repeated the burst pairing protocol in the presence AM251 and the GABA B receptor agonist baclofen (300 nM).…”

Section: Mechanisms Regulating Retrograde Transmitter Releasementioning

confidence: 81%

Dual Regulation of Anterograde and Retrograde Transmission by Endocannabinoids

Iremonger

Kuzmiski²,

Baimoukhametova³

et al. 2011

J. Neurosci.

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Endocannabinoids (eCBs) are feedback messengers in the nervous system that act at the presynaptic nerve terminal to inhibit transmitter release. Here we report that in brain slices from rat, eCBs are released from vasopressin (VP) neurons in the paraventricular nucleus of the hypothalamus following coincident bursts of presynaptic and postsynaptic spiking. eCBs transiently depress glutamate release from excitatory terminals and, in doing so, prevent the synapses from undergoing long-term depression (LTD). Specifically, we show that blockade of CB1 receptors unmasks LTD following coincident presynaptic and postsynaptic activity. This LTD is presynaptic in nature, but requires the release of the opioid peptide dynorphin from the postsynaptic neuron. Dynorphin release and subsequent LTD require the activation of postsynaptic metabotropic glutamate receptors (mGluRs). Our findings indicate that eCBs, by transiently depressing glutamate release, limit mGluR activation and indirectly gate release of dynorphin from the postsynaptic neuron. We propose that eCBs, in addition to their well described role in the rapid modulation of transmitter release from the nerve terminal, also regulate the release of other retrograde transmitters and thus encode for multiple temporal windows of synaptic plasticity.

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Section: Mechanisms Regulating Retrograde Transmitter Releasementioning

confidence: 81%

Dual Regulation of Anterograde and Retrograde Transmission by Endocannabinoids

Iremonger

Kuzmiski²,

Baimoukhametova³

et al. 2011

J. Neurosci.

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“…2003; Gaiarsa et al 1995;Isaacson 1998;Kombian et al 1996;Lei and McBain 2003;Morishita and Sastry 1995;Nisenbaum et al 1992;Wu and Saggau 1995;Yamada et al 1999), including intracortical glutamatergic synapses in the cerebral cortex (Chu and Hablitz 2003;Fukuda et al 1993;Gil et al 1997;Zilberter et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Presynaptic GABA_B Receptors Modulate Thalamic Excitation of Inhibitory and Excitatory Neurons in the Mouse Barrel Cortex

Porter

Nieves

2004

Journal of Neurophysiology

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Porter, James T. and Dalila Nieves. Presynaptic GABA B receptors modulate thalamic excitation of inhibitory and excitatory neurons in the mouse barrel cortex. J Neurophysiol 92: 2762-2770, 2004. First published July 14, 2004 10.1152/jn.00196.2004. Cortical inhibition plays an important role in the processing of sensory information, and the enlargement of receptive fields by the in vivo application of GABA B receptor antagonists indicates that GABA B receptors mediate some of this cortical inhibition. Although there is evidence of postsynaptic GABA B receptors on cortical neurons, there is no evidence of GABA B receptors on thalamocortical terminals. Therefore to determine if presynaptic GABA B receptors modulate the thalamic excitation of layer IV inhibitory neurons and excitatory neurons in layers II-III and IV of the somatosensory "barrel" cortex of mice, we used a thalamocortical slice preparation and patch-clamp electrophysiology. Stimulation of the ventrobasal thalamus elicited excitatory postsynaptic currents (EPSCs) in cortical neurons. Bath application of baclofen, a selective GABA B receptor agonist, reversibly decreased AMPA receptor-mediated and N-methyl-D-aspartate (NMDA) receptor-mediated EPSCs in inhibitory and excitatory neurons. The GABA B receptor antagonist, CGP 35348, reversed the inhibition produced by baclofen. Blocking the postsynaptic GABA B receptormediated effects with a Cs ϩ -based recording solution did not affect the inhibition, suggesting a presynaptic effect of baclofen. Baclofen reversibly increased the paired-pulse ratio and the coefficient of variation, consistent with the presynaptic inhibition of glutamate release. Our results indicate that the presynaptic activation of GABA B receptors modulates thalamocortical excitation of inhibitory and excitatory neurons and provide another mechanism by which cortical inhibition can modulate the processing of sensory information.

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“…Spontaneous unitary synaptic currents (miniatures) obtained in the presence of tetrodotoxin (TTX) were stored on videotape via a pulse-code modulator (Neurodata), detected, and analyzed off-line using Axograph (Axon Instruments). To evoke synaptic responses, a glass stimulating electrode filled with ACSF and connected to an isolated stimulator (Digitimer) was placed in the hypothalamic region dorsomedial to the SON, as described previously (Kombian et al 1996). Synaptic responses were evoked at 0.05 Hz, using square pulses of 0.1-ms duration, and analyzed on-line using pClamp (Axon Instruments).…”

Section: Patch-clamp Recordingmentioning

confidence: 99%

“…Electrophysiological recordings have indicated the presence of functional GABA-A receptors on SON neurons responsible for fast inhibitory potentials (Randle et al 1986). GABA-B receptors have also been reported in the SON on both glutamatergic and GABAergic terminals (Kombian et al 1996;Mouginot et al 1998) and on magnocellular neurons (Harayama et al 1998;Stern et al 2002). Studies performed at the ultrastructural level have revealed that Ͼ40% of all synapses on magnocellular neurons were GABAergic (Gies and Theodosis 1994).…”

Section: Introductionmentioning

confidence: 99%

Dopamine D4 Receptor-Mediated Presynaptic Inhibition of GABAergic Transmission in the Rat Supraoptic Nucleus

Azdad

Piet

Poulain

et al. 2003

Journal of Neurophysiology

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. Dopamine D4 receptor-mediated presynaptic inhibition of GABAergic transmission in the rat supraoptic nucleus. J Neurophysiol 90: 559 -565, 2003; 10.1152/jn.00226.2003. The mechanism by which dopamine induces or facilitates neurohypophysial hormone release is not completely understood. Because oxytocin-and vasopressin-secreting supraoptic neurons are under the control of a prominent GABAergic inhibition, we investigated the possibility that dopamine exerts its action by modulating GABA-mediated transmission. Whole cell voltage-clamp recordings of supraoptic neurons were carried out in acute hypothalamic slices to determine the action of dopamine on inhibitory postsynaptic currents. Application of dopamine caused a consistent and reversible reduction in the frequency, but not the amplitude, of miniature synaptic events, indicating that dopamine was acting presynaptically to reduce GABAergic transmission. The subtype of dopamine receptor involved in this response was characterized pharmacologically. Dopamine inhibitory action was greatly reduced by two highly selective D4 receptor antagonists L745,870 and L750,667 and to a lower extent by the antipsychotic drug clozapine but was unaffected by SCH 23390 and sulpiride, D1/D5 and D2/D3 receptor antagonists, respectively. In agreement with these results, the action of dopamine was mimicked by the potent D4 receptor agonist PD168077 but not by SKF81297 and bromocriptine, D1/D5 and D2/D3 receptor agonists, respectively. Dopamine and PD168077 also reduced the amplitude of evoked inhibitory postsynaptic currents, an effect that was accompanied by an increase in paired-pulse facilitation. These data clearly indicate that D4 receptors are located on GABA terminals in the supraoptic nucleus and that their activation reduces GABA release in the supraoptic nucleus. Therefore dopaminergic facilitation of neurohypophysial hormone release appears to result, at least in part, from disinhibition of magnocellular neurons caused by the depression of GABAergic transmission.

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GABAB receptors presynaptically modulate excitatory synaptic transmission in the rat supraoptic nucleus in vitro

Cited by 77 publications

References 0 publications

Dual Regulation of Anterograde and Retrograde Transmission by Endocannabinoids

Dual Regulation of Anterograde and Retrograde Transmission by Endocannabinoids

Presynaptic GABA_B Receptors Modulate Thalamic Excitation of Inhibitory and Excitatory Neurons in the Mouse Barrel Cortex

Dopamine D4 Receptor-Mediated Presynaptic Inhibition of GABAergic Transmission in the Rat Supraoptic Nucleus

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GABAB receptors presynaptically modulate excitatory synaptic transmission in the rat supraoptic nucleus in vitro

Cited by 77 publications

References 0 publications

Dual Regulation of Anterograde and Retrograde Transmission by Endocannabinoids

Dual Regulation of Anterograde and Retrograde Transmission by Endocannabinoids

Presynaptic GABAB Receptors Modulate Thalamic Excitation of Inhibitory and Excitatory Neurons in the Mouse Barrel Cortex

Dopamine D4 Receptor-Mediated Presynaptic Inhibition of GABAergic Transmission in the Rat Supraoptic Nucleus

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Presynaptic GABA_B Receptors Modulate Thalamic Excitation of Inhibitory and Excitatory Neurons in the Mouse Barrel Cortex