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 unilateral anterior hypothalamus (AH)-lesion mice. Intraperitoneally administered aconitine significantly increased cortical A Ch release within 15 min at 10 and 30 μg/kg. The increasing effect diappeared 30 min after the administration of aconitine. Aconitite-induced ACh release was not inhibited by intracerebroventricularly preadministered atropine (1 and 3 μg/rat). Atropine (1 μg/mouse) preadministered into the contralateral intact AH in mice did not affect aconitine (30 μg/kg, i.p.)-induced bradycardia. These results indicate that the cortical ACh release caused by peripherally administered aconitine dose not occur through activation of the central muscarinic receptor, and thus its ACh release may not be concerned with the occurrence of bradycardia.
