Aconitine induces bradycardia through the transmission pathway involved in anterior hypothalamus in mice

• Published in: Japanese Journal of Pharmacology 1995, Vol.67 (suppl.1), p.136-136
• Main Authors: Takada, Miwako, Makino, Mitsuhiro, Kimura, Ikuko, Kimura, Masayasu
• Format: Article
• Language: English
• ISSN: 0021-5198; 1347-3506
• DOI: 10.1016/S0021-5198(19)46507-4

The aconitine (30 μg/kg, i.p. or 1 μg, i.c.v.)-induced bradycardia is mainly due to centrally acting muscarinic effects. The contribution of the hypothalamus to the effects was investigated by partial lesions of hypothalamus in unanaesthetized mice (7-8 weeks of age, 29-37 g body weight). The lesions were caused by passing direct current (1.5 mA, 13 sec) through the electrode. The mice were used 2 days after the surgery. The bradycardia was prevented (1) by the lesion of hypothalamus except lateral hypothalamus area (n=10), (2) by bilateral lesions of anterior hypothalamus (AH) in 6 out of 10 mice and not (3) by bilateral lesions of the ventromedial, the posterior and the lateral hypothalamus. Bupivacaine (1 μg injected into intact AH), not atropine (1 and 10 μg, injected into intact AH) prevented the bradycardia in 6 out of 11 mice with contralateral lesion of the AH. These results demonstrate that the transmission pathway involved in AH makes contributions to the aconitine (i.p.)-induced bradycardia.