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Noradrenaline depolarization and hyperpolarization mediated by alpha-adrenergic receptors in the soma of dorsal root ganglion neurons

Research paper by Li Zhi-wang, Wang A-jing, Leng Ming, Yang Xiu-ping

Indexed on: 01 Sep '88Published on: 01 Sep '88Published in: Journal of Tongji Medical University = Tong ji yi ke da xue xue bao



Abstract

Intracellular recordings were made on perfused preparation isolated from toad dorsal root ganglion (DRG). Of the 51 neurones examined, 46 were of type A, and the remaining 5 of type C cell. The resting membrane potential of these two types of cells was ™60.06±1.30 mV (\(\bar X\)±SE).When the preparations were superfused with noradrenaline (NA; 10−4 ™ 10−3M), the changes of Rp were as follows: 1) hyperpolarization, with amplitude of 8.38 ± 1.42mV (\(\bar X\)±SE; 20/48); 2) depolarization, with amplitude of 9.39±1.24mv (\(\bar X\)±SE; 23/48); 3) no effect (5/48). The alteration in membrane potential mentioned above could be neither mimicked by application of isoproterenol, nor blocked by propranolol. Therefore, the possibility of the effect being mediated by β-adrenoceptor could be excluded.Application of phenylephrine and clonidine induced depolarization and hyperpolarization of membrane potential respectively, while application of prazosin eand yohimbine blocked depolarization and hyperpolarization response induced by NA, respectively.From the results mentioned above, it may be concluded that depolarization and hyperpolarization induced by NA are mediated by α1- and α2-adrenoceptors on the soma of DRG neurones respectively.