The effect of GHB on electroencephalographic signals has been investigated in animal models and human [14-18]. While acute exposure to exogenous GHB in rats at low doses (50-100 mg/kg) induced immobility and sleep, a hypersynchronous electrographic seizures resembling generalized nonconvulsive epilepsy were observed following GHB at doses higher than 200 mg/kg [15]. These EEG changes were blocked by GABAB receptor antagonists [16]. Chronic exposure to GHB in the rat led to a reduced sleep period reflected by the EEG, and indicated end-organ sensitivity, i.e., tolerance to the hypnotic action of GHB [19].
