Aconitine, a main component of aconite, increases spontaneous acetylcholine release from the frontal cerebral cortex of freely moving rats

Biological & Pharmaceutical Bulletin
I KimuraM Kimura

Abstract

We investigated whether peripherally administered aconitine increases spontaneous acetylcholine (ACh) release from the frontal cerebral cortex in freely moving rats using in vivo microdialysis, as it relates to aconitine-induced bradycardia estimated by a tail-artery cuff technique in unilateral anterior hypothalamus (AH)-lesion mice. Intraperitoneally administered aconitine significantly increased cortical ACh release within 15 min at 10 and 30 micrograms/kg. The increasing effect disappeared 30 min after the administration of aconitine. Aconitine-induced ACh release was not inhibited by intracerebroventricularly preadministered atropine (1 and 3 micrograms/rat). Atropine (1 micrograms/mouse) preadministered into the contralateral intact AH in mice did not affect aconitine (30 micrograms/kg, i.p.)-induced bradycardia. These results indicate that the cortical ACh release caused by peripherally administered aconitine does not occur through activation of the central muscarine receptor, and thus its ACh release may not be concerned with the occurrence of bradycardia.

Citations

Jun 10, 2003·Journal of Applied Toxicology : JAT·Brian M Paddle
Mar 2, 2006·Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan·Ikuko Kimura
Jan 22, 2010·Archives of Pharmacal Research·Cheng PengDing-Kun Zhang

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