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γ-Hydroxybutyrate (GHB) is an endogenous CNS depressant employed in clinical trials for the treatment of narcolepsy and alcohol withdrawal.1 GHB has also become an increasingly popular recreational drug of abuse, presumably because of its sedative/disinhibitory and possible euphoric properties.1,2⇓ GHB inhibits firing of midbrain dopamine neurons, possibly via an action on a unique GHB receptor or on GABAB receptors.1,3⇓ Impaired dopaminergic activity is reflected in experimental biochemical studies by a striking accumulation of striatal dopamine and reduced dopamine metabolite level.1,4⇓ The increased (primarily intraneuronal) dopamine is considered to be consequent to reduced neurotransmitter release and to a short-term acceleration in presynaptic dopamine synthesis compensatory to decreased synaptic levels of the neurotransmitter.1 The ability of GHB to impair acutely dopaminergic neurotransmission has been hypothesized to explain part of the short-lasting sedative action of the drug.1,4⇓ This is supported by animal findings showing that the dopaminergic stimulant amphetamine can reverse part of the immobility caused by GHB.5,6⇓ Conversely, some …
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