| Autor: |
Hanstein R; Institute for Physiological Chemistry and Pathobiochemistry, Department of Pathobiochemistry, Medical School, Johannes Gutenberg-University, Duesbergweg 6, 55099 Mainz, Germany., Lu A, Wurst W, Holsboer F, Deussing JM, Clement AB, Behl C |
| Jazyk: |
angličtina |
| Zdroj: |
Neuroscience [Neuroscience] 2008 Oct 15; Vol. 156 (3), pp. 712-21. Date of Electronic Publication: 2008 Jul 25. |
| DOI: |
10.1016/j.neuroscience.2008.07.034 |
| Abstrakt: |
Corticotropin releasing hormone (CRH) is the central modulator of the mammalian hypothalamic-pituitary-adrenal (HPA) axis. In addition, CRH affects other processes in the brain including learning, memory, and synaptic plasticity. Moreover, CRH has been shown to play a role in nerve cell survival under apoptotic conditions and to serve as an endogenous neuroprotectant in vitro. Employing mice overexpressing murine CRH in the CNS, we observed a differential response of CRH-overexpressing mice (CRH-COEhom-Nes) to acute excitotoxic stress induced by kainate compared with controls (CRH-COEcon-Nes). Interestingly, CRH-overexpression reduced the duration of epileptic seizures and prevented kainate-induced neurodegeneration and neuroinflammation in the hippocampus. Our findings highlight a neuroprotective action of CRH in vivo. This neuroprotective effect was accompanied by increased levels of brain-derived neurotrophic factor (BDNF) in CRH-COEhom-Nes mice, suggesting a potential role for BDNF in mediating CRH-induced neuroprotective actions against acute excitotoxicity in vivo. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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