The regulatory expression of neuronal nitric oxide synthase in the ischemic rat retina

被引:14
作者
Gwon, JS [1 ]
Ju, WK [1 ]
Park, SJ [1 ]
Kim, IB [1 ]
Lee, MY [1 ]
Oh, SJ [1 ]
Chun, MH [1 ]
机构
[1] Catholic Univ Korea, Coll Med, Dept Anat, Seoul 137701, South Korea
关键词
immunocytochemistry; ischemia; neuronal nitric oxide synthase; rat; retina; Western blot;
D O I
10.1097/00001756-200110290-00047
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
We investigated the expression and cellular localization of neuronal nitric oxide synthase (nNOS) in the rat retina, following ischemic injury induced by transient increase of intraocular pressure. In the normal retina, nNOS immunoreactivity was localized to certain populations of amacrine cells, displaced amacrine cells and a few bipolar cells. Following transient ischemia, retinal neurons expressing the immunoreactivity increased and peaked three days after reperfusion. Quantitative evaluation using immunoblotting confirmed that nNOS expression showed a peak value (500% of control levels) at 3 days, and then decreased again to 150% of controls by 4 weeks after reperfusion. Our findings suggest that this overproduced NO may act as a neurotoxic agent in the ischemic rat retina. NeuroReport 12:3385-3389 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:3385 / 3389
页数:5
相关论文
共 25 条
[1]   PROLONGED BILATERAL CAROTID-ARTERY OCCLUSION INDUCES ELECTROPHYSIOLOGICAL AND IMMUNOHISTOCHEMICAL CHANGES TO THE RAT RETINA WITHOUT CAUSING HISTOLOGICAL DAMAGE [J].
BARNETT, NL ;
OSBORNE, NN .
EXPERIMENTAL EYE RESEARCH, 1995, 61 (01) :83-90
[2]   APPARENT HYDROXYL RADICAL PRODUCTION BY PEROXYNITRITE - IMPLICATIONS FOR ENDOTHELIAL INJURY FROM NITRIC-OXIDE AND SUPEROXIDE [J].
BECKMAN, JS ;
BECKMAN, TW ;
CHEN, J ;
MARSHALL, PA ;
FREEMAN, BA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (04) :1620-1624
[3]   Ischemia-induced neuronal apoptosis [J].
Choi, DW .
CURRENT OPINION IN NEUROBIOLOGY, 1996, 6 (05) :667-672
[4]   Light and electron microscopical analysis of nitric oxide synthase-like immunoreactive neurons in the rat retina [J].
Chun, MH ;
Oh, SJ ;
Kim, IB ;
Kim, KY .
VISUAL NEUROSCIENCE, 1999, 16 (02) :379-389
[5]  
DAWON TM, 1994, J NEUROSCI, V14, P5147
[6]   NITRIC-OXIDE SYNTHASE AND NEURONAL NADPH DIAPHORASE ARE IDENTICAL IN BRAIN AND PERIPHERAL-TISSUES [J].
DAWSON, TM ;
BREDT, DS ;
FOTUHI, M ;
HWANG, PM ;
SNYDER, SH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (17) :7797-7801
[7]  
Dawson VL, 1998, PROG BRAIN RES, V118, P215
[8]   NITRIC-OXIDE SYNTHASE INHIBITORS PROTECT RAT RETINA AGAINST ISCHEMIC-INJURY [J].
GEYER, O ;
ALMOG, J ;
LUPUMEIRI, M ;
LAZAR, M ;
ORON, Y .
FEBS LETTERS, 1995, 374 (03) :399-402
[9]   Nitric oxide: A review of its role in retinal function and disease [J].
Goldstein, IM ;
Ostwald, P ;
Roth, S .
VISION RESEARCH, 1996, 36 (18) :2979-2994
[10]   A comparison of the effects of L-NAME, 7-NI and L-NIL on carrageenan-induced hindpaw oedema and NOS activity [J].
Handy, RLC ;
Moore, PK .
BRITISH JOURNAL OF PHARMACOLOGY, 1998, 123 (06) :1119-1126