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.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002395:Catecholamines / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects; D004298:Dopamine / Q000494:pharmacology; D006885:Hydroxybutyrates / Q000494:pharmacology*; D009474:Neurons / Q000187:drug effects; D009638:Norepinephrine / Q000494:pharmacology; D011817:Rabbits; D011956:Receptors, Cell Surface / Q000187:drug effects*; D011963:Receptors, GABA-A; D012978:Sodium Oxybate / Q000494:pharmacology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D002395:Catecholamines; D006885:Hydroxybutyrates; D011956:Receptors, Cell Surface; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid; D012978:Sodium Oxybate; D004298:Dopamine; D009638:Norepinephrine