The muscarinic receptor agonist oxotremorine methiodide evokes a nicotinic response in mammalian sympathetic neurons

Evidence for muscarinic M4 receptors mediating nonadrenergic noncholinergic relaxations in rabbit anococcygeus muscle

“…This is shown for carbachol, oxotremorine M, cis-dioxolane and (+)-muscarine in Fig. 4, demonstrating the mixed cholinergic action (muscarinic/nicotinic) of carbachol and oxotremorine M. These results are consistent with the nicotinic properties of oxotremorine M and carbachol as observed at mammalian sympathetic neurons (Xian et al 1994;Boksa et al 1989). In contrast, cis-dioxolane was less potent as nicotinic agonist and (+)-muscarine exhibited a pure muscarinic activity in the concentration range tested.…”

Activation of M1 Muscarinic Receptors Triggers Transmitter Release from Rat Sympathetic Neurons Through an Inhibition of M‐Type K+ Channels

“…OxoM has been found to activate nAChRs in Xenopus myocytes (Reitstetter et al 1994) and in guinea‐pig coeliac ganglion neurons (Xian et al 1994). To verify whether nAChRs might contribute to the secretagogue action of OxoM in rat sympathetic neurons, tritium overflow was stimulated by electrical fields, OxoM (100 μ m ), and DMPP (100 μ m ) in either the absence or presence of 10 μ m of the nicotinic antagonist mecamylamine (Fig.…”

“…OxoM is generally considered a pure muscarinic receptor agonist with some preference for the M 2 subtype (Caulfield, 1993). Nevertheless, evidence has been presented that OxoM may also activate nAChRs in either Xenopus myocytes (Reitstetter et al 1994) or guinea‐pig neurons (Xian et al 1994). In rat SCG neurons, as shown here, OxoM was able to induce inward currents at negative membrane potentials at concentrations > 100 μ m , and these currents were abolished by the nAChR antagonist mecamylamine.…”

Muscarinic M1receptors activate phosphoinositide turnover and Ca2+mobilisation in rat sympathetic neurones, but this signalling pathway does not mediate M‐current inhibition

“…Oxo‐M (10 μ m ) can evoke nicotinic currents in sympathetic neurones (Xian et al 1994), and the influx of calcium through nicotinic receptor channels can significantly elevate intraneuronal calcium (Trouslard et al 1993). Since muscarinic receptor stimulation of PLC can be markedly enhanced by procedures which increase intracellular calcium (Baird & Nahorski, 1989; Fisher et al 1989; del Río et al 1994), we tested whether nicotinic calcium elevation may have contributed to the stimulatory effect of oxo‐M on PLC activity.…”