The effects of quisqualic acid lesions of the nucleus basalis magnocellularis on short-term memory capacities of the rat have been investigated using the delayed matching and non-matching to position tasks. The lesions do not disrupt performance of either task by pretrained animals, but do disrupt the ability to acquire the non-matching contingency, and to reverse to the non-matching task when trained on the matching task. The unidirectional nature of the reversal deficit has been replicated. The generalized disruption of performance of either task by the muscarinic antagonist scopolamine was comparable in lesioned and control rats. The lesions were associated with extensive loss of acetylcholinesterase staining in the basal forebrain and in the neocortex, and 55% depletions of choline acetyltransferase activity in the neocortex but not in the hippocampus. These observations demonstrate that the cholinergic projection from nucleus basalis to the neocortex is not critical for normal short-term memory, but that lesions involving this system do disrupt specific types of conditional discrimination learning.