SPATIAL-LEARNING DISABILITY IN RATS WITH FOCAL CEREBRAL-ISCHEMIA RECOVERS BY REPEATING MORRIS WATER MAZE TESTS

Citation
Y. Kumon et al., SPATIAL-LEARNING DISABILITY IN RATS WITH FOCAL CEREBRAL-ISCHEMIA RECOVERS BY REPEATING MORRIS WATER MAZE TESTS, Biomedical research, 16(6), 1995, pp. 423-431
Citations number
18
Categorie Soggetti
Medicine, Research & Experimental
Journal title
ISSN journal
03886107
Volume
16
Issue
6
Year of publication
1995
Pages
423 - 431
Database
ISI
SICI code
0388-6107(1995)16:6<423:SDIRWF>2.0.ZU;2-8
Abstract
The effect of repeated Morris water maze tests on the ability of place navigation was examined in rats with permanent unilateral occlusion o f the middle cerebral artery (MCA) and/or the ipsilateral common carot id artery (CCA), in relation to choline acetyltransferase (ChAT) immun oreactivity in the basal magnocellular nucleus of Meynert (NBM). The M orris water maze task was conducted 2, 4, 6 and 8 weeks after MCA or M CA/CCA occlusion; each test included two trials per day for 4 days, an d the mean latency for the rats to reach an invisible platform below t he water surface was measured. MCA- or MCA/CCA-occluded rats subjected to repeated water maze tests exhibited only transient disability of p lace-navigation; the mean latency of MCA- or MCA/CCA-occluded rats bec ame close to that of sham-operated rats by 6 to 8 weeks after ischemia . Despite the time-dependent recovery of place-navigation activity in MCA- or MCA/CCA-occluded rats, ChAT neurons in the NBM, which are cons idered to be involved primarily in spatial learning ability, were fewe r on the ischemic side than on the non-ischemic side throughout the ex amination period. Moreover, hemispheric atrophic changes were prominen t at later stages after MCA or MCA/CCA occlusion. These findings sugge st that early water maze training facilitates the functional restorati on of MCA- or MCA/CCA-occluded rats, and that the recovery of place-na vigation activity in the ischemic rats cannot necessarily be explained by a reduction in the ischemic injury of ChAT neurons in the NBM.