AIM: To study the effects of huperzine A an nucleus basalis magnocellu
laris (NBM) lesion-induced spatial working memory impairment. METHODS:
A delayed-non-match-to-sample radial arm maze task was used to study
spatial working memory. ?he choline acetyltransferase (ChAT) activity
was determined by the conversion of [H-3]acetyl-CoA to [H-3]ACh. RESUL
TS: Unilateral NBM lesion by kainic acid 0.02 mu mol impaired rat's ab
ility to perform this working memory task as; evidenced by fewer corre
ct choices after different delay intervals and more total errors to co
mplete the task. This behavioral impairment associated with a decrease
in the activity of ChAT by about 40% in the ipsilateral cerebral cort
ex. Huperzine A (0.2 mg . kg(-1) ip 30 min before testing) ameliorated
this spatial working memory impairment. Physostigmine (0.2 - 0.3 mg .
kg(-1) ip 20 min before testing) also attenuated the NBM lesion-induc
ed memory deficit. CONCLUSION: The integrity of NBM, is critical for s
patial working memory processing, and this working memory impairment i
nduced by NBM lesion can be ameliorated by huperzine A and physostigmi
ne.