ACONITINE INDUCES BRADYCARDIA THROUGH A TRANSMISSION PATHWAY INCLUDING THE ANTERIOR HYPOTHALAMUS IN CONSCIOUS MICE

Citation
I. Kimura et al., ACONITINE INDUCES BRADYCARDIA THROUGH A TRANSMISSION PATHWAY INCLUDING THE ANTERIOR HYPOTHALAMUS IN CONSCIOUS MICE, Biological & pharmaceutical bulletin, 20(8), 1997, pp. 856-860
Citations number
22
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
0918-6158
Volume
20
Issue
8
Year of publication
1997
Pages
856 - 860
Database
ISI
SICI code
0918-6158(1997)20:8<856:AIBTAT>2.0.ZU;2-I
Abstract
Aconitine administered intraperitoneally (i.p.) produces bradycardia m ainly bg a central muscarinic action. The involvement of hypothalamic regions in the occurrence of aconitine-induced bradycardia was investi gated in hypothalamus-lesioned mice. The lesions were made by passing a direct current (1.5 mA, 13 s) through a monopolar electrode, The aco nitine (30 mu g/kg, i.p.)-induced bradycardia was prevented by bilater al lesions of either the whole hypothalamus, except for the lateral hy pothalamus area, or the anterior hypothalamus (AH), The bradycardia wa s not prevented by bilateral lesions of the ventromedial, the paravent ricular, the posterior or the lateral hypothalamus regions. Bupivacain e, but not atropine(1 mu g, administered into the intact AH) prevented aconitine-induced bradycardia in mice with a contralaterally lesioned AH. Aconitine (0.8 mu g) directly administered into the unilateral AH in intact mice caused a late phase and lesser extent of bradycardia. These results suggest that a transmission pathway including the AH con tributes to the aconitine-induced bradycardia but does not involve the activation of muscarinic receptors in the AH.