The influence of sodium gamma-hydroxybutyrate on GABA receptors and catecholamine effect potentiation.

The effects of microiontophoretically applied gamma-hydroxybutyric acid and gamma-hydroxybutyrate (GHBA-Na) on the extracellularly registered spontaneous neuronal electrical activity of rabbit's sensorimotor and frontal cerebral cortex were studied. GHBA-Na depressed the firing of cortical neurons in a dose-dependent manner. This effect was blocked by bicuculline. It was concluded that GHBA-Na interacted with GABA receptors of the neuronal membrane. During traumatic epilepsy GHBA-Na caused excitation of cortical neurons and showed antagonistic relationships with GABA. It is supposed that during epilepsy GHBA-Na binds with GABA receptors, decreases competitively the effect of natural GABA and thus it might cause a disinhibition of neurons. GHBA-Na increased and prolongated the depression of the neurons of frontal cortex which was caused by microiontophoretical application of catecholamines: dopamine and norepinephrine. It is suggested that GHBA-Na prevents catecholamines inactivation.