Alzheimer's disease is a progressive dementia associated with cholinergic cell loss in the nucleus of Meynert that induces deficiencies in cholinergic neurotransmission in the neocortex. The nucleus basalis magnocellularis (NBM) is the rodent homologue to the nucleus of Meynert in humans. In this study, we examined the effects of GM1 ganglioside, a neuroprotective agent, on morphological and functional recovery after electrolytic or ibotenic acid lesions of the NBM. In animals, GM1 ganglioside has been shown to reduce some of the behavioral deficits that follow Central Nervous System lesions. Electrolytic or ibotenic acid lesions produced deficits in passive avoidance learning, as assessed by the number of trails taken to acquire the avoidance response. Only the electrolytic lesions impaired spatial memory in the Morris Water Maze (MWM), and GM1 administration did not improve performance on this task. Facilitation of passive avoidance acquisition was observed in animals receiving GM1 treatment after electrolytic or ibotenate lesions. Both types of injuries induced equivalent amounts of damage to the nucleus basalis but the electrolytic lesions produced greater damage to adjacent structures that could be responsible for the additional deficits observed on the MWM task.