tatCN19o. CPC Scientific; Coultrap et al. 2011. N/A (custom peptide).
Abstract
Learning and memory are thought to require hippocampal long-term potentiation (LTP), a form of synaptic plasticity that is persistently impaired after cerebral ischemia and that requires movement of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) to excitatory synapses. We show here that oxygen/glucose-deprivation (OGD) in cultures hippocampal neurons causes a long-lasting impairment of CaMKII movement. Notably, CaMKII inhibition at 30 min after onset of OGD prevented the impairment in CaMKII movement. Thus, CaMKII mediates both, LTP mechanisms and their ischemia-induced impairment. These findings provide a mechanism by which ischemic conditions can impair LTP and explain how CaMKII inhibition after cerebral ischemia can prevent these LTP impairments.
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