Studies Upon the Mechanism by Which Acetylcholine Releases Surplus Acetylcholine in a Sympathetic Ganglion

Abstract

1Acetylcholine (ACh) releases surplus ACh from the superior cervical ganglion of the cat and the experiments described in this paper tested whether this results from exchange of endogenous ACh with exogenous ACh; the experiments also attempted to characterize pharmacologically the mechanism of this action of ACh.

Nicotinic mechanisms in the autonomic control of organ systems

“…In the ANS virtually every neuron contains transcripts for nAChRs subunits (Skok and Selianko, 1978;Chang and Berg, 1999;Kristufek et al, 1999), and nAChRs are located on both pre-and postsynaptic terminals (Collier and Katz, 1975;Briggs and Cooper, 1982;Langer, 1997). The nAChRs located presynaptically facilitate both spontaneous and evoked ACh release (Coggan et al, 1997;Liang and Vizi, 1997), whereas the postsynaptic receptors are the main mediators of ganglionic fast synaptic transmission (Selyanko et al, 1979;Fieber and Adams, 1991;Trouslard et al, 1993;Conroy and Berg, 1995).…”

Nicotine Potentiates the Electrical Field Stimulation-Evoked Contraction of Non-Pregnant Rabbit Myometrium

“…The presynaptic nicotinic acetylcholine receptors (nAchRs) have been shown to play a role in the modulation of the release of neurotransmitters (Collier and Katz 1975). The ganglionic nAchRs have also been reported to be involved in the release of neurotransmitters because nicotine-induced release of Ach from the myenteric plexus (Torocsik et al 1991) or nicotine-induced release of dopamine from the rat striatum (Marshall et al 1996) was abolished by tetrodotoxin (TTX) which is a blocker of sodium channels.…”