Abstract:
:Dentate gyrus is usually assumed to be resistant to ischemia. However, the mechanisms underlying this functional plasticity are not fully understood. Herein, we aimed at identifying a neuroprotective mechanism in the dentate gyrus of the adult rat after global ischemia. Cyclic AMP response element (CRE)-binding protein (CREB), brain-derived neurotrophic factor (BDNF) and calcium/calmodulin-dependent protein kinase IV (CaMKIV) are known to be mediators of neuronal survival and plasticity. Involvement of CaMKIV, BDNF and CREB in ischemic resistance was therefore examined using intracerebroventricular injections of pharmacological agents such as inhibitors, antibodies and consensus oligonucleotides followed by immunohistochemical and Western blot analysis. We provide evidence that ischemia triggers activation of a biphasic pathway during the resistance period of dentate neurons: (1) CaMKIV mediates the early phosphorylation of CREB which drives a prominent synthesis of BDNF; (2) this BDNF synthesis, in turn, induces a second peak of CREB phosphorylation which is required for the maintenance of BDNF synthesis. In addition, we show that: (1) impairment of these transduction signals by the pharmacological agents causes tissular damages and apoptotic deaths in the post-ischemic dentate gyrus; (2) some similar disturbances also occur beyond the resistance period in the dentate gyrus of untreated ischemic rats; (3) these disturbing effects are mainly observed in the suprapyramidal dentate subfield. Collectively, the present results suggest that activation of the CaMKIV/CREB/BDNF pathway plays principally an early protective role in the suprapyramidal subfield of the dentate gyrus.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Blanquet PR,Mariani J,Fournier Bdoi
10.1016/j.expneurol.2006.06.016subject
Has Abstractpub_date
2006-12-01 00:00:00pages
357-72issue
2eissn
0014-4886issn
1090-2430pii
S0014-4886(06)00392-Xjournal_volume
202pub_type
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