Munakata M, Fujimoto M, Akaike N, Araki H
Department of Physiology, Kyushu University Faculty of Medicine, Fukuoka, Japan.
Neuroreport. 1996 Jan 31;7(2):613-6. doi: 10.1097/00001756-199601310-00057.
We investigated the effects of VA-045 ((+)-eburnamenine-14 carboxylic acid (2-nitroxyethyl) ester) on GABA(A) receptor-mediated Cl- currents in dissociated rat cerebral cortical neurones, using a nystatin-perforated patch recording configuration. At a holding potential of - 40mV, the external application of GABA evoked an inward Cl- current with an EC50 value of 5.6 x 10(-6)M. VA-045 increased the GABA response at GABA concentrations below 3.0 x 10(-6)M. The GABA response showed a time dependent decay consisting of fast and slow components and VA-045 significantly accelerated both components. The site of action for VA-045 was considered to be different from that for benzodiazepines or barbiturates.