NMDA>D-CPP>NMDA/CPP>NMDA/SCH-23390
The present experiment tested interactions between NAC NMDA and D1 receptor ligands on PFC ACh efflux. Results indicate that intra-NAC perfusion of 150 or 250 uM NMDA similarly increase (143-187%) cortical ACh release. Co-administration of the D1 antagonist SCH-23390 (150 uM) markedly attenuated the increase observed follwoing the lower concentration of NMDA (by 80%) but only marginally dampened (by 16%) the effects of the higher concentration of NMDA. Second, we determined whether the D1 agonist SKF-81297 (200 uM) would potentiate the effects of a low concentration of NMDA (75 uM) that does not increase cortical ACh when administered alone. Results indicate that this is not the case. The D1 antagonist data indicate that activation of D1 receptors potentiates ACh release induced by low concentrations of NMDA but such modulation is not necessary following higher NMDA concentrations. The initial D1 agonist data suggest this positive modulation is not sufficient to render a subthreshold concentration of NMDA, with respect to ACh release, to an above threshold level.
"Modulation of cortical acetylcholine release via glutamatergic and D1 interactions in the nucleus accumbens." A. Zmarowski1, M. Sarter2, and J.P. Bruno1. Department of Psychology, Ohio State University1, Columbus, OH 43210 and University of Michigan2, Ann Arbor, MI 48109.