4.6 Article

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

期刊

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
卷 44, 期 5, 页码 1801-1810

出版社

SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2019.4353

关键词

transient global cerebral ischemia; hyperpolarization- activated cyclic nucleotide-gated channel; astrocyte; pericyte; hippocampus; delayed neuronal death

资金

  1. 'Cooperative Research Program for Agriculture Science and Technology Development' Rural Development Administration, Republic of Korea [PJ01321101]
  2. National Research Foundation of Korea (NRF) - Ministry of Science, ICT & Future Planning [NRF-2017R1A2B4009079]
  3. NRF - Ministry of Education [NRF-2017R1D1A1B03029311]

向作者/读者索取更多资源

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.

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