Quinolinic Acid-Induced Decreases in Acetylcholine Release in the Rat Nucleus Basalis Magnocellularis

Abstract

The tryptophan metabolite quinolinic acid (Quin) is a potent agonist at N-methyl-D-aspartate (NMDA) receptors on central cholinergic neurons in the rat nucleus basalis magnocellularis (nbM; Stone and Connick, 1985). Quin injected into the nbM produces neuronal death and axon-sparing lesions of this cortically projecting pathway (Schwarcz and Köhler, 1983; Stone and Connick, 1985). The effects of such lesions on cortical cholinergic parameters have indicated that this pathway provides the major cholinergic input to the rat frontoparietal cortex. Both morphological and electrophysiological evidence suggests that the cholinergic neurons located in the nbM also provide local cholinergic input to this area of the brain in the form of axon collaterals (Lamour et al., 1986; Semba et al., 1987). Recently, we have shown that the release of acetylcholine (ACh) in the nbM can be stimulated by potassium depolarization and in addition requires calcium for optimal release of ACh (Metcalf and Boegman, 1987). In the present study, we used Quin to produce lesions of the nbM, then determined the effect of these lesions on the release of endogenous ACh from tissue slices prepared from the nbM.