ACTIVATION OF GABA-A RECEPTOR IN THE BRAIN SUPPRESSES NEOSTIGMINE OR HISTAMINE-INDUCED CENTRAL NERVOUS SYSTEM-MEDIATED HYPERGLYCEMIA

We investigated the effect of GABA receptor agonists on the central ne rvous system (CNS)-mediated hyperglycemia induced by neostigmine or hi stamine in anesthetized fed rats. The injection of muscimol, GABA(A) r eceptor agonist (1, 2.5 nmol) into the third cerebral ventricle suppre ssed the hyperglycemia induced by intraventricular injection of neosti gmine (1x10(-8) mol) or histamine (5x10(-7) mol) . Baclofen, GABA(B) r eceptor agonist (1, 2.5 nmol) , however, did not suppress these hyperg lycemia. Neither muscimol nor baclofen (2.5 nmol) affected plasma gluc ose levels. These findings suggest that activation of GABA(A) receptor in the CNS suppresses the hyperglycemia induced by the stimulation of cholinoceptive neuron or histaminergic neuron, but activation of GABA (B) receptor does not affect them.