Enriched environment reverse learning impairment after focal cerebral ischemia in rats

P. Dahlqvist, A. Rönnbäck and T. Olsson

Department of Medicine, Umeå University Hospital, Umeå, Sweden

Stroke is a major cause of death in the industrialized world. However, most stroke victims survive with varying degree of disability. Within the first months, significant functional improvement occurs in most stroke survivors, which can be further enhanced by rehabilitation. This is likely to be attributable to plastic changes in the brain outside the ischemic lesion, which are modulated by experiences. However, the neurobiological mechanisms of stroke recovery are largely unknown.

Cognitive impairment is a common and highly disabling symptom after stroke. This is reflected by impaired spatial learning and memory in rodent stroke models using middle cerebral artery occlusion (MCAo). Housing in an enriched environment (EE), i.e. group housing in a large cage with ladders and toys that are changed daily, enhance brain plasticity and improve recovery of sensorimotor functions after experimental stroke in rats.

We have used the Morris water maze to investigate if postischemic EE-housing can attenuate the spatial memory impairment after MCAo in rats. After MCAo Male Sprague Dawley rats were randomized to EE or a deprived environment. Sensorimotor function was tested weekly for four weeks and on day 31-34 after MCAo spatial learning was tested in the Morris water maze.

MCAo resulted in major difficulties finding the hidden platform, with increased thigmotaxis behaviour. The learning impairment was positively correlated with the brain infarct volume. Post ischemic housing in EE significantly improved function in the water maze, but did not reduce infarct volume. Furthermore EE housing extinguished the association between spatial learning and infarct volume.

We conclude that EE-housing after MCAo and the Morris water maze are useful models in the search of putative molecular mediators of improved cognitive recovery and plasticity after stroke. We are pursuing this mediator-search, aiming to better understand the neurobiological mechanisms underlying recovery after brain ischemia with the explicit aim to develop new therapies enhancing functional recovery in stroke patients.


Paper presented at Measuring Behavior 2005 , 5th International Conference on Methods and Techniques in Behavioral Research, 30 August - 2 September 2005, Wageningen, The Netherlands.

© 2005 Noldus Information Technology bv