The effect of coniine on presynaptic nicotinic receptors

• Published in: Zeitschrift für Naturforschung C. A journal of biosciences Vol. 71; no. 5; pp. 115 - 120
• Main Authors: Erkent, Ulkem, Iskit, Alper B., Onur, Rustu, Ilhan, Mustafa
• Format: Journal Article
• Language: English
• Published: Germany De Gruyter 01-05-2016
• Subjects: Alkaloids - toxicity; Animals; anococcygeus; atrium; coniine; Dose-Response Relationship, Drug; Guinea Pigs; Heart Atria - metabolism; Male; Muscle, Skeletal - metabolism; Myocardium - metabolism; nicotine; nicotinic receptors; nitric oxide; Piperidines - toxicity; Rats; Receptors, Nicotinic - metabolism; Synapses - metabolism; Synaptic Transmission - drug effects
• ISSN: 0939-5075; 1865-7125
• DOI: 10.1515/znc-2015-0194

Toxicity of coniine, an alkaloid of
(poison hemlock), is manifested by characteristic nicotinic clinical signs including excitement, depression, hypermetria, seizures, opisthotonos via postsynaptic nicotinic receptors. There is limited knowledge about the role of presynaptic nicotinic receptors on the pharmacological and toxicological effects of coniine in the literature. The present study was undertaken to evaluate the possible role of presynaptic nicotinic receptors on the pharmacological and toxicological effects of coniine. For this purpose, the rat anococcygeus muscle and guinea-pig atria were used
. Nicotine (100 μM) elicited a biphasic response composed of a relaxation followed by contraction through the activation of nitrergic and noradrenergic nerve terminals in the phenylephrine-contracted rat anococcygeus muscle. Coniine inhibited both the nitrergic and noradrenergic response in the muscle (–logIC
= 3.79 ± 0.11 and –logIC
= 4.57 ± 0.12 M, respectively). The effect of coniine on nicotinic receptor-mediated noradrenergic transmission was also evaluated in the guinea-pig atrium (–logIC
= 4.47 ± 0.12 M) and did not differ from the –logIC
value obtained in the rat anococcygeus muscle. This study demonstrated that coniine exerts inhibitory effects on nicotinic receptor-mediated nitrergic and noradrenergic transmitter response.