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短暂性脑缺血后沙鼠海马 CA1 亚区锥体神经元中 HCN 通道的改善及其在内皮细胞和星形胶质细胞中的新表达水平。

Improved HCN channels in pyramidal neurons and their new expression levels in pericytes and astrocytes in the gerbil hippocampal CA1 subfield following transient ischemia.

机构信息

Department of Anatomy, College of Korean Medicine, Dongguk University, Gyeongju, Gyeongbuk 38066, Republic of Korea.

Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung‑Wonju National University, Gangneung, Gangwon 25457, Republic of Korea.

出版信息

Int J Mol Med. 2019 Nov;44(5):1801-1810. doi: 10.3892/ijmm.2019.4353. Epub 2019 Sep 26.

Abstract

Hyperpolarization‑activated cyclic nucleotide‑gated (HCN) channels have been known to participate in the regulation of neuronal excitability, synaptic transmission and long‑term potentiation in the hippocampus. The present study investigated transient ischemia‑induced changes of HCN1 and HCN2 expressions in the Cornu Ammonis 1 (CA1) subfield of the hippocampus in gerbils subjected to 5 min transient global cerebral ischemia (tgCI). Neuronal death was exhibited in pyramidal neurons of the striatum pyramidale in the CA1 subfield 4 days after tgCI. HCN1 and HCN2 immunoreactivities were demonstrated in intact CA1 pyramidal neurons, and were transiently and markedly increased in the CA pyramidal neurons at 6 h after ischemia. Thereafter, they gradually decreased in a time‑dependent manner. A total of 4 days after ischemia, HCN1 and HCN2 immunoreactivities were barely detected in the CA1 pyramidal neurons; however, HCN1 and HCN2 were began to be expressed in pericytes and astrocytes at 4 days after ischemia. The results indicated that HCN1 and HCN2 expression levels were apparently changed in the gerbil hippocampal CA1 subfield following tgCI and suggested that ischemia‑induced alterations in HCN1 and HCN2 expression levels may be closely associated with the death of CA1 pyramidal neurons following 5 min of tgCI.

摘要

超极化激活环核苷酸门控 (HCN) 通道已被证实参与调节海马神经元的兴奋性、突触传递和长时程增强。本研究探讨了短暂性全脑缺血 (tgCI) 后沙鼠海马 CA1 区 HCN1 和 HCN2 表达的短暂变化。tgCI 后 4 天,在 CA1 区的纹状体锥体神经元中出现了神经元死亡。HCN1 和 HCN2 免疫反应性在完整的 CA1 锥体神经元中显示,在缺血后 6 小时,CA 锥体神经元中短暂且明显增加。此后,它们呈时间依赖性逐渐减少。缺血后 4 天,CA1 锥体神经元中几乎检测不到 HCN1 和 HCN2 免疫反应性;然而,在缺血后 4 天,HCN1 和 HCN2 开始在周细胞和星形胶质细胞中表达。结果表明,tgCI 后沙鼠海马 CA1 区的 HCN1 和 HCN2 表达水平明显改变,提示缺血诱导的 HCN1 和 HCN2 表达水平的改变可能与 5 分钟 tgCI 后 CA1 锥体神经元的死亡密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86ce/6777693/d9de47aa3eea/IJMM-44-05-1801-g00.jpg

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