| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4344705 | Neuroscience Letters | 2012 | 6 Pages |
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 2 h during and 1 d 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 2 h during and 1 d after PISE. CRF was induced in calbindin (CB) or calretinin (CR) immunoreactive interneurons in stratum oriens at 2 h 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.
► CRF was studied in pilocarpine model of status epilepticus (PISE). ► CRF was up-regulated significantly in the hippocampus at 2 h during and 1 d after PISE. ► CRF may be related to excitoneurotoxicity and delayed loss of hippocampal neurons.
