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Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14676-80. doi: 10.1073/pnas.0907842106. Epub 2009 Aug 10.

Postischemic PKC activation rescues retrograde and anterograde long-term memory.

Author information

1
Blanchette Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV 26505, USA. mksun@brni-jhu.org

Abstract

Therapeutics for cerebral ischemia/hypoxia, which often results in ischemic stroke in humans, are a global unmet medical need. Here, we report that bryostatin-1, a highly potent protein kinase C (PKC) activator, interrupts pathophysiological molecular cascades and apoptosis triggered by cerebral ischemia/hypoxia, enhances neurotrophic activity, and induces synaptogenesis in rats. This postischemic therapeutic approach is further shown to preserve learning and memory capacity even 4 months later as well as long-term memory induced before the ischemic event. Our results of electromicroscopic and immunohistochemical analyses of neuronal and synaptic ultra-structure are consistent with a PKC-mediated synaptic remodeling and repair process that confers long-lasting preservation of spatial learning and memory before and after the cerebral ischemic/hypoxic event, suggesting a previously undescribed therapeutic modality for cerebral ischemia/hypoxia and ischemic stroke.

PMID:
19667190
PMCID:
PMC2732881
DOI:
10.1073/pnas.0907842106
[Indexed for MEDLINE]
Free PMC Article
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