FIG 6.

Transient hypoxia ischemia (tHI)-induced calcineurin-dependent GAP43-S41 dephosphorylation and GAP43-gephyrin association in developing neurons. Neonatal P2 rat pups were subjected to unilateral tHI or sham operation, and both contralateral (Cont) and ipsilateral (Ipsi) cerebral cortex were subjected to Western blotting of pGAP43/GAP43 in total cell lysate (A) and co-IP for GAP43-Geph association (B). (Top) representative blot; (bottom) quantification graph. The graph in panel B illustrates the data from each individual (left) and the compiled data (right). An unpaired t test was used for panel A and the compiled data in panel B (*, P < 0.05; **, P < 0.01 versus sham treatment), and paired t test was used for the individual data graph in panel B (*, P < 0.05; ns, not significant); n = 5. (C and D) Transient oxygen-glucose deprivation (tOGD), an in vitro tHI model, was applied to 4-DIV cortical neurons for 1 h, followed by 23 h of recovery under normal oxygen/glucose conditions with or without the calcineurin inhibitor FK506 (1 μM). Cell lysate WB for pGAP43-S41 and total GAP43 (C) and co-IP of GAP43 and Geph (D) were performed. ##, P < 0.01 versus tOGD; n = 4.