Marrosu F, Giagheddu M, Gessa G L, Fratta W
Institute of Neurology, University of Cagliari, Italy.
Epilepsia. 1992 May-Jun;33(3):435-8. doi: 10.1111/j.1528-1157.1992.tb01687.x.
Studies have shown that intracerebroventricular (i.c.v.) injection (10-20 micrograms) of corticotropin releasing factor (CRF) in rats induces epileptiform activity characterized by a regular (pacemaker-like) spiking pattern located in hippocampal leads. CRF has also been shown to increase the firing rate of noradrenergic neurons in the locus ceruleus. Our experiments clarified the possible role of norepinephrine (NE) in mediating hippocampal activity of CRF. Intraperitoneal (i.p.) injection of the alpha 2-agonist clonidine at a dose of 0.5-5 micrograms/kg prevented, in a dose-related manner, the hippocampal epileptiform activity induced by CRF (20 micrograms i.c.v.). Our results suggest a possible role of NE in CRF-induced spiking activity.
研究表明,向大鼠脑室内(i.c.v.)注射(10 - 20微克)促肾上腺皮质激素释放因子(CRF)会诱发癫痫样活动,其特征为海马导联中出现规则的(类似起搏器的)尖峰模式。CRF还被证明可提高蓝斑中去甲肾上腺素能神经元的放电频率。我们的实验阐明了去甲肾上腺素(NE)在介导CRF海马活动中的可能作用。腹腔内(i.p.)注射剂量为0.5 - 5微克/千克的α2 - 激动剂可乐定,以剂量相关的方式预防了由CRF(20微克i.c.v.)诱导的海马癫痫样活动。我们的结果表明NE在CRF诱导的尖峰活动中可能发挥作用。