摘要
提取大鼠大脑皮层突触膜并与丁螺环酮6.2 5～ 4 0 0 0 μmol·L- 1直接孵育 ,放射免疫法测定cAMP含量 ,发现丁螺环酮可浓度依赖地提高cAMP产生量 ,说明腺苷酸环化酶 (AC)活性升高 .神经生长因子 2 ,10kU·L- 1,三环类抗抑郁剂地昔帕明2 .5 ,5 μmol·L- 1或丁螺环酮 5 ,10 ,2 0 μmol·L- 1分别与皮质酮 0 .2mmol·L- 1共孵PC12细胞 4 8h ,均可防止皮质酮所致的PC12神经细胞损伤 ,使存活细胞增多 .结果提示丁螺环酮激活信号转导系统AC cAMP通路 ,从而对损伤神经元产生保护作用 ,这可能与其抗抑郁 ,抗焦虑作用有关 .
The synaptic membrane extracted from the cerebral cortex of rats was incubated directly with buspirone 6.25-4000 μmol·L -1 for 10 min, then cAMP content was detected by radio-immunoassay. The results showed that buspirone raised the cAMP production in a concentration-dependent manner, which suggest that buspirone activate adenylate cyclase(AC). After incubation with nerve growth factor 2,10 kU·L -1, buspirone 5, 10, 20 μmol·L -1 or desipramine 2.5, 5 μmol·L -1, respectively in the presence of corticosterone 0.2 mmol·L -1 for 48 h, the number of surviving PC12 cells was increased, which suggest that treatment with the drugs protect cells from the lesion by corticosterone. It indicates that buspirone activates the AC-cAMP pathway in signal transduction system, there by protecting neurons from the lesion. These two aspects maybe partly consisted of the antidepressant and anxiolytic mechanism of buspirone.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
2001年第5期333-336,共4页
Chinese Journal of Pharmacology and Toxicology
