Abstract

This chapter reviews the studies in which the effects of endogenous and exogenous nitric oxide (NO) on the release of acetylcholine were investigated. As tools for the involvement of endogenous NO, the effects of NO synthase inhibitors on release of acetylcholine were studied. The cholinergic neurons are tonically stimulated by endogenous NO. On the other hand, NO synthase inhibitors fail to change either basal or electrically evoked acetylcholine release from slices of rat hippocampus and striatum. Endogenous and exogenous NO increase basal acetylcholine release from central and peripheral cholinergic neurons. The effect is tetrodotoxin sensitive and calcium-dependent, thus reflecting stimulation of exocytotic release. The facilitation of acetylcholine release is likely to be mediated via the cGMP system. In addition, NO has been shown to decrease the action potential-evoked acetylcholine release from peripheral neurons. The mechanism of inhibition is not known. Contraction experiments on various intestinal preparations suggest that the presynaptic nitrergic inhibition of acetylcholine release has functional consequences.

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