EXPRESSION OF BAX AND BCL-2 PROTEIN IN THE GERBIL HIPPOCAMPUS FOLLOWING TRANSIENT FOREBRAIN ISCHEMIA AND ITS MODIFICATION BY PHENCYCLIDINE

To determine the effect of phencyclidine (a noncompetitive NMDA recept or antagonist) on expression of Bax and Bcl-2 (apoptosis-regulating pr oteins) in gerbil hippocampus after transient forebrain ischemia, brai n sections were immunohistochemically evaluated 48, 72, 96 h and 7 day s following ischemia. In ischemic control animals, the expression of B ax in CA1 neurons was increased with time and peaked at 72 h, then dis appeared at 96 h. In the phencyclidine (5 mg kg(-1), intraperitoneally )-treated animals, the intensity of Bax expression at 72 h was weaker than that of ischemic control animals. Furthermore, at 96 h, Bax expre ssion was still observed in CA1 neurons. No expression of Bcl-2 in the CA1 neurons was detected in either control or phencyclidine-treated a nimals. From these results, it is possible that NMDA receptor antagoni sts exert their preventive effect against delayed neuronal death throu gh inhibition of Bax protein expression, although the precise relation ship between the function of Bax protein and delayed neuronal death is still unclear.