Elsevier

Neuroscience Letters

Volume 409, Issue 3, 6 December 2006, Pages 187-191
Neuroscience Letters

Ischemic preconditioning-induced activation of ERK1/2 in the rat hippocampus

https://doi.org/10.1016/j.neulet.2006.09.053Get rights and content

Abstract

We investigated the activation and cellular localization of the extracellular signal-regulated kinases ERK1/2 in a rat model of ischemic tolerance induction. Adult male Sprague–Dawley rats were subjected to 3 min of sublethal ischemic preconditioning. Activation of ERK1/2 showed the characteristic time- and cell-dependent patterns. Rapid and short-lasting activation of ERK after 3 min of cerebral ischemia was noted immediately in the dentate granule cells and mossy fibers of the hippocampus, and then occurred sequentially in CA3 and CA1 neurons and dentate hilar neurons at 10 min. Phosphorylation of ERK1/2 in hippocampal neurons returned to the basal level in an ordered manner. Basal level phosphorylation was attained first, at 30 min, by the CA1 neurons, and was then observed in CA3 and granule cells by 1 h and noted in some dentate hilar neurons at 12 h. By contrast, phosphorylation of ERK1/2 in mossy fibers and the CA1 dendritic field was sustained for at least 3 d. Transient activation of ERK1/2 was induced also in astrocytes of the dentate hilar region at 1 d post-stimulation. These data demonstrate that the short cerebral-ischemic preconditioning induced rapid and transient activation of ERK1/2 in tolerance-acquired CA1 neurons as well as in ischemia-resistant CA3 and dentate granule cells, and that the short preconditioning sustained activation in mossy fibers and neuropil areas, suggesting that ERK1/2 activation may be involved in the mechanism of ischemic tolerance in the rat hippocampus.

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Acknowledgements

This research was supported by a grant (M103KV010010-06K2201-01010) from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, the Republic of Korea. We gratefully acknowledge the technical assistance to Mr. Hong Lim Kim.

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