Department of Anatomy, College of Medicine, Soonchunhyang University, Cheonan, Korea.
BMB Rep. 2012 Nov;45(11):635-40. doi: 10.5483/bmbrep.2012.45.11.091.
To understand the effects of HCN as potential mediators in the pathogenesis of epilepsy that evoke long-term impaired excitability; the present study was designed to elucidate whether the alterations of HCN expression induced by status epilepticus (SE) is responsible for epileptogenesis. Although HCN1 immunoreactivity was observed in the hippocampus, its immunoreactivities were enhanced at 12 hrs following SE. Although, HCN1 immunoreactivities were reduced in all the hippocampi at 2 weeks, a re-increase in the expression at 2-3 months following SE was observed. In contrast to HCN1, HCN 4 expressions were un-changed, although HCN2 immunoreactive neurons exhibited some changes following SE. Taken together, our findings suggest that altered expressions of HCN1 following SE may be mainly involved in the imbalances of neurotransmissions to hippocampal circuits; thus, it is proposed that HCN1 may play an important role in the epileptogenic period as a compensatory response.
为了了解 HCN 作为可能的介导物在引起长期兴奋性受损的癫痫发病机制中的作用，本研究旨在阐明癫痫持续状态（SE）诱导的 HCN 表达改变是否与癫痫发生有关。尽管在海马体中观察到 HCN1 免疫反应性，但在 SE 后 12 小时其免疫反应性增强。尽管在 2 周时所有海马体中的 HCN1 免疫反应性均降低，但在 SE 后 2-3 个月观察到表达再次增加。与 HCN1 相反，HCN4 的表达没有改变，尽管 SE 后 HCN2 免疫反应性神经元发生了一些变化。总之，我们的发现表明 SE 后 HCN1 的表达改变可能主要涉及到海马回路神经递质传递的失衡；因此，有人提出 HCN1 可能在癫痫发生期作为代偿反应发挥重要作用。
