J. Puolivali et al., Apolipoprotein E-deficient mice are not more susceptible to the biochemical and memory deficits induced by nucleus basalis lesion, NEUROSCIENC, 96(2), 2000, pp. 291-297
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.