Effect of cholinesterase inhibitors on Morris water task behavior following lesions of the nucleus basalis magnocellularis.

Abstract

The effect of bilateral nucleus basalis magnocellularis (nBM) lesions on performance in the Morris water task was examined in the rat, and the ability of anticholinesterase inhibitors to reverse the behavioral deficit was evaluated. Lesions of nBM resulted in a prolongation of escape latency. A spatial probe trial revealed that animals with sham lesions swam a greater percentage of the distance in the platform quadrant; this finding was abolished by nBM lesions. Lesions of nBM produced a nonsignificant increase in both open-field activity and activity-box scores. In Experiment 1, administration of 0.32 mg/kg physostigmine on Day 3 only resulted in a decrease in escape latency. In Experiment 2, in which cholinesterase inhibitors were administered daily for 5 days, 0.32 mg/kg but not low-dose physostigmine or two substituted N,N-alkyl phenyl carbamate cholinesterase inhibitors (RA-6 and RA-7) again improved escape latency on Day 3. Thus it was concluded that nBM lesions impair behavior on the Morris water task and physostigmine shortens escape latency.