Noebels J L, Rutecki P A
Department of Neurology, Baylor College of Medicine, Houston, TX 77030.
Brain Res. 1990 Aug 6;524(2):225-30. doi: 10.1016/0006-8993(90)90695-8.
A latent, gene-linked alteration of hippocampal network excitability in tg/tg mutant mice was unmasked in vitro by convulsant-activated synchronous neuronal discharges. Exposure to elevated extracellular potassium ions or 4-aminopyridine, but not picrotoxin, revealed an abnormally prolonged network discharge duration in the mutant CA3 pyramidal cell region. In both phenotypes, noradrenaline, and a selective beta-noradrenergic receptor agonist, isoproterenol, reversibly accelerated the frequency of the discharges. These findings identify an intrinsic alteration in the excitability of an isolated neuronal network in a model of inherited generalized spike-wave epilepsy, and further implicate noradrenergic mechanisms in the temporal modulation of hippocampal synchronization and epileptogenesis.
惊厥激活的同步神经元放电在体外揭示了tg/tg突变小鼠海马网络兴奋性的潜在基因连锁改变。暴露于细胞外钾离子升高或4-氨基吡啶，但不是印防己毒素，显示突变体CA3锥体细胞区域的网络放电持续时间异常延长。在两种表型中，去甲肾上腺素和选择性β-去甲肾上腺素能受体激动剂异丙肾上腺素可逆地加速放电频率。这些发现确定了遗传性全身性棘波癫痫模型中孤立神经元网络兴奋性的内在改变，并进一步表明去甲肾上腺素能机制参与海马同步化和癫痫发生的时间调制。
