just parking this here.....
Nippon Yakurigaku Zasshi 1999 Feb;113(2):85-95
[Availability of 2VO rats as a model for chronic cerebrovascular disease].
[Article in Japanese]
Nanri M, Watanabe H
Department of Pharmacology, Toyama Medical and Pharmaceutical University, Japan.
[Medline record in process]
We have established a chronic cerebral hypoperfusion model that is produced by permanent occlusion of bilateral common
carotid arteries (2VO) in rats. 2VO rats exhibited rarefaction in the white matter, shrinkage of neurons in the cerebral cortex
and hippocampus 1-3 days after 2VO and infarctions in the striatum 7 days after 2VO. These histological changes in the cortex
and hippocampus were accompanied by a decrease in immunoreactivity for microtubule-associated protein 2 (MAP2).
Immunoreactivity for glial fibrillary acid protein (GFAP) was observed at 3-7 days after 2VO. Marked increase in GFAP
staining in astrocytes in the cerebral cortex and hippocampus was found 30 days after ligation. In the 8-arm radial maze
performance, the 2VO rats showed a higher rate of errors than the sham-operated control during repeated training periods.
THA (9-amino-1,2,3,4-tetrahydroacridine), a cholinesterase inhibitor and GTS-21 (3-(2,4-dimethoxybenzylidene)-anabaseine
dihydrochloride), a central nicotinic acetylcholine-receptor agonist improved the learning impairment in the radical maze task of
2VO rats. GTS-21 administration exerted a protective effect against the neuropathological changes that followed 2VO. Taken
together, the 2VO rat appears to be a useful model for investigating the pathophysiology of human dementia and to elucidate
the therapeutic potential of drugs for this disease. |
