Two types of calcium channels regulating activation of proline-rich tyrosine kinase 2 induced by transient brain ischemia in rat hippocampus.

Tyrosine phosphorylation is an important means for regulating post-ischemic signal transduction. In this article, brain ischemia was induced by four-vessel occlusion, and the effect of ischemia/reperfusion on proline-rich tyrosine kinase 2 (Pyk2) was studied. Tyrosine phosphorylation of Pyk2 in Sprague–Dawley rat hippocampus after transient (15 min) brain ischemia and reperfusion was examined by immunoprecipitation and immunoblot. Kinase activity of Pyk2 was examined by the method of 32P-incorporation into poly(Glu-Tyr). Tyrosine phosphorylation and kinase activity of Pyk2 decreased slightly after ischemia, then increased after reperfusion and reached the peak levels (5.1 and 1.8 times the levels of the sham-operated group, respectively) at 1 h of reperfusion. Both the increases were partly inhibited by NMDA receptor antagonist ketamine and L-type voltage-gated calcium channel antagonist nifedipine administered 20 min before ischemia. The results suggested that Pyk2 was activated after transient brain ischemia and reperfusion, and it might play an important role in mediating post-ischemic signal transduction events.