Department of Biochemistry, Kunming Medical College, Kunming, PR China.
Neurosci Lett. 2012 Mar 23;512(2):83-8. doi: 10.1016/j.neulet.2012.01.057. Epub 2012 Feb 4.
We investigated the cellular localization and progressive changes of corticotropin releasing factor (CRF) in the mouse hippocampus, during and after pilocarpine induced status epilepticus (PISE) and subsequent epileptogenesis. We found that CRF gene expression was up-regulated significantly at 2h during and 1d after PISE in comparison to control mice. Immunohistochemical analysis showed that the number of CRF and Fos immunoreactive cells was increased significantly in the strata oriens and pyramidale of CA1 area and in the stratum pyramidale of CA3 area at 2h during and 1d after PISE. CRF was induced in calbindin (CB) or calretinin (CR) immunoreactive interneurons in stratum oriens at 2h during PISE. It suggests that induced CRF may be related to the over excitation of hippocampal neurons and occurrence of status epilepticus. It may also cause excitoneurotoxicity and delayed loss of CA3 and CA1 pyramidal neurons, leading to the onset of epilepsy.
我们研究了在匹罗卡品诱导的癫痫持续状态（PISE）期间和之后，应激激素释放因子（CRF）在小鼠海马中的细胞定位和渐进性变化，以及随后的癫痫发生。我们发现，与对照组小鼠相比，CRF 基因表达在 PISE 期间的 2 小时和之后的 1 天显著上调。免疫组织化学分析显示，在 CA1 区的层状或锥体和 CA3 区的层状锥体中，CRF 和 Fos 免疫反应细胞的数量在 PISE 期间的 2 小时和之后的 1 天显著增加。在 PISE 期间的 2 小时，CRF 诱导了在 calbindin（CB）或 calretinin（CR）免疫反应性中间神经元中的层状。这表明诱导的 CRF 可能与海马神经元的过度兴奋和癫痫持续状态的发生有关。它也可能导致兴奋毒性和 CA3 和 CA1 锥体神经元的延迟丢失，从而导致癫痫的发生。
