PMID: 9427965Jan 15, 1998Paper

Expression of Bax and Bcl-2 protein in the gerbil hippocampus following transient forebrain ischemia and its modification by phencyclidine

Neurological Research
M NiwaT Uematsu

Abstract

To determine the effect of phencyclidine (a noncompetitive NMDA receptor antagonist) on expression of Bax and Bcl-2 (apoptosis-regulating proteins) in gerbil hippocampus after transient forebrain ischemia, brain sections were immunohistochemically evaluated 48, 72, 96 h and 7 days following ischemia. In ischemic control animals, the expression of Bax in CA1 neurons was increased with time and peaked at 72 h, then disappeared 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 expression was still observed in CA1 neurons. No expression of Bcl-2 in the CA1 neurons was detected in either control or phencyclidine-treated animals. From these results, it is possible that NMDA receptor antagonists exert their preventive effect against delayed neuronal death through inhibition of Bax protein expression, although the precise relationship between the function of Bax protein and delayed neuronal death is still unclear.

Citations

Dec 24, 2002·Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology·Haiyun XuXin-Min Li
Apr 19, 2002·The Journal of Pharmacology and Experimental Therapeutics·Justin McInnisKenneth M Johnson
Jul 25, 2000·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·J ChenS H Graham
Jun 16, 2004·Journal of Neuroscience Research·Jingxin QiuJ Regino Perez-Polo
Jun 17, 2000·Progress in Neurobiology·K J BanasiakG G Haddad
Mar 27, 2003·Progress in Neuro-psychopharmacology & Biological Psychiatry·Seth Love
Feb 3, 2005·Reproductive Toxicology·William SlikkerCheng Wang

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