Abstract
The effect of gamma-hydroxybutyric acid (GHB) on the excitatory postsynaptic potential (EPSP) evoked in thalamocortical neurones of the rat dorsal lateral geniculate nucleus and ventrobasal thalamus was investigated in vitro. GHB (0.1-5 mM) dose-dependently and reversibly decreased (36-78%) the amplitude of the sensory EPSP. This effect of GHB was blocked by the GABAB receptor antagonist CGP 35348 (1 mM). NCS 382 (1-3 mM), a putative GHB receptor antagonist, did not antagonise but weakly potentiated both the GHB- and baclofen-mediated decrease of the EPSP amplitude.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adjuvants, Anesthesia / pharmacology*
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Animals
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Anticonvulsants / pharmacology
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Baclofen / pharmacology
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Benzocycloheptenes / pharmacology
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Bicuculline / pharmacology
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Dose-Response Relationship, Drug
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Electrophysiology
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GABA Agonists / pharmacology
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GABA Antagonists / pharmacology
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GABA-B Receptor Agonists*
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Geniculate Bodies / cytology*
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Male
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Neurons, Afferent / chemistry
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Neurons, Afferent / physiology
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Organophosphorus Compounds / pharmacology
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Presynaptic Terminals / chemistry
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Presynaptic Terminals / physiology
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Rats
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Rats, Wistar
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Receptors, GABA-B / physiology
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Sodium Oxybate / pharmacology*
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Synaptic Transmission / drug effects*
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Synaptic Transmission / physiology
Substances
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Adjuvants, Anesthesia
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Anticonvulsants
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Benzocycloheptenes
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GABA Agonists
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GABA Antagonists
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GABA-B Receptor Agonists
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Organophosphorus Compounds
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Receptors, GABA-B
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NCS 382
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Sodium Oxybate
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CGP 35348
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Baclofen
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Bicuculline