当前位置： SCI文献检索 > NEUROSCIENCE LETTERS期刊下所有文献 > N-methyl-D-aspartate receptor and L-type voltage-gated Ca2+ channel activation mediate proline-rich tyrosine kinase 2 phosphorylation during cerebral ischemia in rats.

N-methyl-D-aspartate receptor and L-type voltage-gated Ca2+ channel activation mediate proline-rich tyrosine kinase 2 phosphorylation during cerebral ischemia in rats.

Abstract：

:Cerebral ischemia induces rapid efflux of glutamate into the extracellular space contributing to excessive activation of glutamate receptors in postsynaptic cells, particularly N-methyl-D-aspartate (NMDA) receptors, which triggers the neuron lesion through calcium overload. Our studies indicated that cerebral ischemia stimulated the rapid activation of nonreceptor tyrosine kinases proline-rich tyrosine kinase 2 (Pyk2) and Src and the binding to Pyk2 activated the latter. Pyk2 activation significantly depends on the increase of the intracellular calcium level; blockage of both calcium ion channel NMDA receptors and L-type voltage-gated Ca2+ channel (L-VGCC), respectively, could effectively inhibit phosphorylation of Pyk2 in early ischemia episodes. Moreover, pretreatment with the protein kinase C inhibitor (chelerythrine chloride) reduced the ischemia-induced activation of Pyk2. Noticeably, CaMKII, a family of calcium/calmodulin-dependent kinases, also may be involved in the regulation of Pyk2 activity because its inhibitor KN62 attenuated Pyk2 phosphorylation during ischemia. Together with previous studies, these results indicate that calcium influx elicited by active NMDA receptors and L-VGCC triggers the Pyk2-Src signaling pathway mediated by PKC, which aggravates cerebral ischemia lesions through up-regulating the function of NMDA receptors after the onset of ischemia, and also could be regulated partly by CaM-dependent kinases like CaMKII.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Guo J,Meng F,Fu X,Song B,Yan X,Zhang G

doi

10.1016/j.neulet.2003.10.076

keywords:

subject

Has Abstract

pub_date

2004-01-30 00:00:00

pages

177-80

issue

3

eissn

0304-3940

issn

1872-7972

pii

S030439400301320X

journal_volume

355

pub_type

杂志文章

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