Identification of G alpha subtype(s) involved in gamma-aminobutyric acid(B) receptor-mediated high-affinity guanosine triphosphatase activity in rat cerebral cortical membranes

The ability of a series of specific G alpha carboxyl-terminal antisera, (i. e, anti-Gs alpha, anti-Gi1/2 alpha, anti-Gi3 alpha /Go alpha, anti-Go alpha /Gi3 alpha, and anti-Gq/11 alpha) to disrupt (+/-)-baclofen-stimulated hig h-affinity guanosine triphosphatase (GTPase) activity was explored in rat c erebral cortical membranes to identify the G alpha subunit(s) involved in g amma -aminobutyric acids (GABA(B)) receptor-mediated signal transduction. P retreatment of the membranes with the AS/7 (anti-Gi1/2 alpha) antiserum inh ibited GABA(B) receptor-mediated response without affecting the basal activ ity. The RM/1 (anti-Gs alpha) and QL (anti-Gq/11 alpha) antisera failed to inhibit GABA(B) receptor-coupled responses. The results of the EC/2 (anti-G i3 alpha /Go alpha) and GO/1 (anti-Go alpha /Gi3 alpha) antisera were diffi cult to interpret since the basal activities were influenced by these antis era. These results, in conjunction with the data in our previous reconstitu tion study, indicate that Gi2 alpha is a main transducer of GABA(B) recepto r-mediated signaling in rat cerebral cortex. (C) 2001 Elsevier Science irel and Ltd. All rights reserved.