PMID: 11313294Apr 21, 2001Paper

GHB depresses fast excitatory and inhibitory synaptic transmission via GABA(B) receptors in mouse neocortical neurons

Cerebral Cortex
K Jensen, I Mody

Abstract

Gamma-hydroxybutyrate (GHB) is a drug of abuse which induces sedation and euphoria. However, overdoses can severely depress the level of consciousness or can be fatal especially when combined with other substances. Studies have suggested that the GHB-effects are mediated via actions on thalamocortical pathways and local neocortical circuits, although the effect of GHB at the level of single neocortical neurons is not clear. Using whole-cell patch-clamp recordings, we studied the effects of GHB on neocortical neurons in brain slices from 12- to 33-day-old mice. We found that GHB depressed the frequency and amplitude of GABAergic and glutamatergic spontaneous inhibitory and excitatory post-synaptic currents (IPSCs and EPSCs) driven by presynaptic action potential firing, while the amplitude and frequency of Ca(2+) entry-independent miniature IPSCs were not affected. Using minimal stimulation, GHB reduced the probability of release at inhibitory synapses onto neocortical layer 2/3 pyramidal cells. Also, GHB directly hyperpolarized layer 2/3 non-pyramidal cells by up to 11 mV and inhibited action potential firing. All these effects of GHB were mediated via GABA(B)-receptors. In conclusion, GHB activates both pre- and postsynaptic G...Continue Reading

Citations

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