Inducible nitric oxide synthase induces beta-amyloid neurotoxicity in vivo.
- Author:
Hui LIU
1
;
Jun-pao CHEN
;
Wan-qin ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Alzheimer Disease; metabolism; pathology; Amyloid beta-Peptides; metabolism; toxicity; Animals; Guanidines; pharmacology; Indazoles; pharmacology; Male; Maze Learning; Nitric Oxide; metabolism; Nitric Oxide Synthase; antagonists & inhibitors; Nitric Oxide Synthase Type II; metabolism; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2002;18(4):329-332
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the causative role of nitric oxide synthase (NOS) and nitric oxide (NO) in neurotoxicity of beta-amyloid (Abeta) and the pathogenesis of Alzheimer's disease (AD).
METHODSUsing behavioral and neuropathological methods, we observed the effects of Abeta(1-40) injection into hippocampi on rats learning and memory in Y maze and on the neuropathology in hippocampi. The intervention by intraperitoneal administration of aminoguanidine (AG), a selective inducible NOS (iNOS) inhibitor, and 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor, in the neurotoxicity of Abeta(1-40) was studied then.
RESULTSThe capability of acquisition and retrieval in Y maze and local neurons in hippocampus of the rats were impaired significantly after Abeta(1-40) injection. Intraperitoneal administration of AG, but not 7-NI, could prevent the damages caused by Abeta(1-40) injection above-mentioned.
CONCLUSIONiNOS/NO participates in the mechanisms of Abeta-induced neurotoxicity and may play an important role in the pathogenesis of AD.
