GAMMA-HYDROXYBUTYRIC ACID (GHB) AND NEUROENDOCRINE FUNCTION IN HUMANS

Gamma hydroxybutyric acid (GHB) has been demonstrated to suppress etha nol withdrawal symptoms in rats and humans. Contrasting data have been reported about GHB mechanism of action. A variety of studies suggest for GHB GABA-like activity, dopamine release reduction, increased dopa mine concentration in the brain or serotonine stimulating action. We i nvestigated in 12 healthy male volunteers (age 25, 2+/-3, 5) B-EP, ACT H, GH, PRL, LH, TSH and Cortisol responses to oral GHB (Alcover CT-Ita ly), acutely administered, at the dose of 25 mg/kg body weight. GH lev els showed a significant increase (p < 0,005), PRL, BEP, ACTH and Cort isol levels a slight not significant increase after GHB. LH and TSH di dn't show any change after GHB administration. No hormonal changes wer e induced by placebo administration. Blood pressure and heart rate nor mal values have been demonstrated during the tests. GH levels rise can be considered as a GABAergic effect of GHB. GHB failure to inhibit AC TH and Cortisol secretion, as expected by GABAergic drugs, suggests a specific mechanism of action for GHB. The involvement of a subpopulati on of GABA receptors (GHB specific receptors) may be hypothesized. At these doses GHB do not show a dopaminergic effect; PRL increase eviden ced by others after high doses GHB i.v. administration can be attribut able to an aspecific hypotensive stress reaction. Our study exclude GH B effects on thyroid function or hypothalamo pituitary gonadal axis.