The effects of NBM- lesion on synaptic plasticity in rats

Abstract

The nucleus basalis magnocellularis (NBM) is a major source of cholinergic projections to the neocortex that is vulnerable to degeneration in Alzheimer's disease. Despite numerous anatomical, pharmacological, behavioral, and physiological investigations of NBM, there is no in vivo study of its effects on short- or long-term synaptic plasticity. Hence, this study was devoted to the assessment of the effects of bilateral lesion of the NBM on synaptic plasticity in the dentate gyrus of the hippocampus using electrophysiological techniques. For this purpose, twenty-five male Wistar rats were randomly allocated into the three Control, Sham, and NBM-lesioned groups. Lesion was made via bilateral injections of 5µg/µl ibotenic acid. After twenty-one days, the input–output functions, paired-pulse facilitation/inhibition, and long-term potentiation (LTP) were evaluated in the dentate gyrus while the perforant pathway was stimulated. NBM lesion was found to attenuate the basal synaptic responsiveness, paired-pulse responses, and LTP in the rats’ dentate gyrus, indicating that lesions of this cholinergic nucleus affects both short- and long-term neural plasticity in the dentate gyrus although NBM does not send direct cholinergic projections to the hippocampus.