抄録
A conitine administered intraperitoneally (i.p.) produces bradycardia mainly by a central muscarinic action. The involvement of hypothalamic regions in the occurrence of aconitine-induced bradycardia was investigated in hypothalamus-lesioned mice. The lesions were made by passing a direct current (1.5mA, 13s) through a monopolar electrode. The aconitine (30 μg/kg, i.p.)-induced bradycardia was prevented by bilateral lesions of either the whole hypothalamus, except for the lateral hypothalamus area, or the anterior hypothalamus (AH). The bradycardia was not prevented by bilateral lesions of the ventromedial, the paraventricular, the posterior or the lateral hypothalamus regions. Bupivacaine, but not atropine (1 μg, administered into the intact AH) prevented aconitine-induced bradycardia in mice with a contralaterally lesioned AH. Aconitine (0.8 μg) 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 contributes to the aconitine-induced bradycardia but does not involve the activation of muscarinic receptors in the AH.
