The regulatory expression of neuronal nitric oxide synthase in the ischemic rat retina.
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 over-produced NO may act as a neurotoxic agent in the ischemic rat retina.
Gwon
J S
JS
Department of Anatomy, College of Medicine, The Catholic University of Korea, 505 Banpo-dong, Socho-gu, Seoul 137-701, Korea.
Ju
W K
WK
Park
S J
SJ
Kim
I B
IB
Lee
M Y
MY
Oh
S J
SJ
Chun
M H
MH
D000818:Animals; D002545:Brain Ischemia / Q000201:enzymology* / Q000503:physiopathology; D016923:Cell Death / Q000502:physiology*; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D007429:Intraocular Pressure / Q000502:physiology; D008297:Male; D009410:Nerve Degeneration / Q000201:enzymology / Q000503:physiopathology; D009474:Neurons / Q000201:enzymology* / Q000473:pathology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000201:enzymology* / Q000503:physiopathology; D012160:Retina / Q000201:enzymology* / Q000293:injuries / Q000503:physiopathology; D015854:Up-Regulation / Q000502:physiology
D009569:Nitric Oxide; D019001:Nitric Oxide Synthase