作者: Ami P. Raval , Kunjan R. Dave , Daria Mochly-Rosen , Thomas J. Sick , Miguel A. Pérez-Pinzón
DOI: 10.1523/JNEUROSCI.23-02-00384.2003
关键词:
摘要: Glutamate receptors and calcium have been implicated as triggering factors in the induction of tolerance by ischemic preconditioning (IPC) brain. However, little is known about signal transduction pathway that ensues after IPC pathway. The main goals present study were to determine whether NMDA induces via a promotes translocation protein kinase C e (ePKC) isozyme this PKC key We corroborate here sublethal dose neuroprotective, whereas blockade during diminished IPC-induced neuroprotection. Calcium chelation blocked protection afforded both significantly, suggesting significant role calcium. Pharmacological with nonselective activator phorbol myristate acetate could not emulate IPC, but activation chelerythrine its These results suggested there might be dual involvement isozymes IPC. This was corroborated when neuroprotection we inhibited ePKC preconditioning, emulated ePKC. possible correlation between NMDA, Ca2+, found diacylglycerol analog oleoylacetyl glycerol, an indirect which Ca2+ activate calcium-insensitive isozyme. demonstrated played IPC- NMDA-induced tolerance.