Apolipoprotein E-deficient mice are not more susceptible to the biochemical and memory deficits induced by nucleus basalis lesion

We investigated whether the nucleus basalis lesion induced by quisqualic ac id was associated with a more severe impairment of spatial navigation in a water maze, a greater reduction in frontal choline acetyltransferase activi ty and decrease in the number of choline acetyltransferase-positive neurons in the nucleus basalis in apolipoprotein E-deficient mice than in control mice. We also studied the effect of ageing on water maze spatial navigation and cortical choline acetyltransferase activity in 16-month-old control an d apolipoprotein E-deficient mice. We found that the lesion decreased choli ne acetyltransferase-positive neurons in the nucleus basalis and frontal ch oline acetyltransferase activity equally in control and apolipoprotein E-de ficient mice. The nucleus basalis lesion had no effect on the initial acqui sition in the water maze in control and apolipoprotein E-deficient mice aft er 25 or 106 days of recovery. However, the nucleus basalis lesion impaired the reversal learning in the water maze similarly in both strains after 25 days of recovery, but had no effect after 106 days of recovery. Finally, w ater maze spatial navigation and cortical choline acetyltransferase activit y were similar in old control and apolipoprotein E-deficient mice. These results suggest that young and old apolipoprotein E-deficient mice do not have impairments in cholinergic activity or spatial navigation. Furthe rmore, apolipoprotein E deficiency does not increase the sensitivity to cho linergic and spatial navigation deficits induced by lesioning of the nucleu s basalis with an excitatory amino acid and does not slow down the behavior al recovery. (C) 2000 IBRO. Published by Elsevier Science Ltd.