Aaltonen_1991_Pharmacol.Biochem.Behav_39_563

Bilateral quisqualic acid nucleus basalis (NB) lesions impaired passive avoidance (PA) retention. NB lesions did not impair acquisition performance (stable platform location) in the water maze (WM). However, NB-lesioned rats were impaired in learning the new location of the escape platform in WM. Pretraining injections of tacridine (an anticholinesterase, THA) at 3 mg/kg, but not at 1 mg/kg, slightly improved PA retention performance in NB-lesioned rats. THA (1 or 3 mg/kg) did not alleviate NB lesion-induced WM defect. The results further suggest that loss of NB neurons impair PA acquisition and relearning of the new platform location in WM, and that cholinergic neuron loss may be at least partially involved in the NB lesion-induced performance defect.