Differences in memory impairment and response to GM1 ganglioside treatmentfollowing electrolytic or ibotenic acid lesions of the nucleus basalis magnocellularis

Alzheimer's disease is a progressive dementia associated with cholinergic c ell loss in the nucleus of Meynert that induces deficiencies in cholinergic neurotransmission in the neocortex. The nucleus basalis magnocellularis (N BM) is the rodent homologue to the nucleus of Meynert in humans. In this st udy, we examined the effects of GM 1 ganglioside, a neuroprotective agent, on morphological and functional recovery after electrolytic or ibotenic aci d 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 avoidan ce learning, as assessed by the number of trials taken to acquire the avoid ance response. Only the electrolytic lesions impaired spatial memory in the Morris Water Maze (MWM), and GM1 administration did not improve performanc e 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 s tructures that could be responsible for the additional deficits observed on the MWM task.