Corcoran M E, Mason S T
Brain Res. 1980 May 26;190(2):473-84. doi: 10.1016/0006-8993(80)90289-9.
The rate and pattern of seizure development provoked by repeated electrical stimulation of the amygdala (kindling) was assessed in rats that had been pretreated with intracerebral injections of the selective catecholaminergic neurotoxin 6-hydroxy-dopamine. Rats with selective depletion of forebrain noradrenaline displayed a highly significant facilitation of both primary-site and secondary-site kindling, whereas no such effect occurred in rats with selective depletion of forebrain dopamine. The facilitative effects of noradrenaline depletion were apparently related to disinhibition of the spread of seizure discharge from the stimulated site rather than to increased epileptogenicity in the stimulated site itself. These results are consistent with previous evidence that noradrenaline reduces the susceptibility of the central nervous system to epileptiform activity, and they suggest that a lessening of seizure-suppressant noradrenergic function in the forebrain might be part of the mechanism underlying kindling.
在预先经脑内注射选择性儿茶酚胺能神经毒素6-羟基多巴胺处理的大鼠中，评估了反复电刺激杏仁核（点燃）诱发癫痫发作的速率和模式。前脑去甲肾上腺素选择性耗竭的大鼠在初级位点和次级位点的点燃均表现出高度显著的促进作用，而在前脑多巴胺选择性耗竭的大鼠中未出现这种效应。去甲肾上腺素耗竭的促进作用显然与癫痫放电从刺激位点的扩散去抑制有关，而不是与刺激位点本身的致痫性增加有关。这些结果与先前的证据一致，即去甲肾上腺素降低中枢神经系统对癫痫样活动的易感性，并且它们表明前脑抑制癫痫发作的去甲肾上腺素能功能减弱可能是点燃潜在机制的一部分。
