Actions of polypeptides at the neuromuscular junction

Abstract

The effects of several polypeptides, e.g. angiotensin II, substance P, oxytocin and vasopressin, on the isolated frog gastrocnemius, chick biventer cervicis and rat hemodiaphragm preparations were studied using electrophysiological and neurochemical techniques. The effects of angiotensin II, substance P, oxytocin and vasopressin on neuromuscular transmission and muscle contraction were investigated by studying the following parameters: the directly and indirectly-elicited twitch and tetanic contractions, nerve compound action potential, uptake of 3H-methylcholine into nerve-muscle preparations, the contractures produced by depolarizing drugs, e.g. ACh or TEA. The results showed that angiotensin II (10(-10)-10(-6) M) and substance P (10(-7)-10(-6) M) enhanced neuromuscular transmission and muscle contraction by increasing the amplitudes of the indirectly-elicited twitch and tetanic contractions. Oxytocin and vasopressin (1-100 mU/ml-1) both depressed neuromuscular transmission by reducing the contractile and electrical response in the frog, chick and rat skeletal muscle. It was concluded that, like their effects on ganglionic transmission, the peptides can modify neuromuscular transmission. The mechanism by which these peptides produce their effects may be dependent on external calcium concentration. These peptides may affect both pre- and postjunctional mechanisms; prejunctionally by increasing/decreasing the release of ACh, and postjunctionally by affecting the sensitivity of the postjunctional membrane to depolarizing drugs and/or producing a contracture in the skeletal muscle.

Muscles innervated by a single motor neuron exhibit divergent synaptic properties on multiple time scales

“…Further, from presynaptic transmitter release to the regulation of contraction machinery, all aspects of the neuromuscular transform are subject to neuromodulation and thus can differ according to the behavioral state of the organism (Brezina, 2010;Brezina et al, 2000;Hooper and Weaver, 2000;Williams et al, 2013;Worden, 1998). Given the prevalence of neuromodulators acting on muscles, including in the STNS (Brezina, 2010;Fort et al, 2004;Hooper et al, 1999;Jorge-Rivera and Marder, 1996;Jorge-Rivera et al, 1998;Wali, 1985;Weimann et al, 1997;Worden, 1998;Wu and Cooper, 2012), it is possible that there are modulatory conditions in which the balance of depression and facilitation, and the properties of augmentation between the three muscles may converge. Similarly, relaxation kinetics are modulated, and the differences in summation between the three muscles could converge under a particular modulatory environment (Jing et al, 2010;Jorge-Rivera et al, 1998).…”