Abstract
Background: The nucleus basalis magnocellularis (NBM) sends projections to the hippocampus that are implicated in learning and memory formation. Despite ample evidence proposing that cognitive function impairment related to neurodegeneration, it may result from alteration of biochemical substances. We aimed to investigate the effects of NBM lesions on the hippocampal interleukin-1beta (IL-1β), brain-derived neurotrophic factor (BDNF), and corticosterone levels, as inflammation markers, and hallmarks of neurodegeneration, stress, and metabolic status. Methods: Thirty-six male Wistar rats were randomly put in control, sham, and NBM-lesioned groups. After inducing the lesion using an intra-NBM injection of 10 μg ibotenic acid (5 μg/μL, each side) in rats, memory was estimated using the passive avoidance test. Moreover, serum and hippocampal IL-1β levels, as well as the hippocampal corticosterone, BDNF, and glucose levels were measured after 42 days. Results: Findings indicated a significant impairment of retention at different intervals in the NBM-lesioned group. BDNF decreased whereas corticosterone, glucose, and IL-1β levels increased in the hippocampus. Also, the levels of serum IL-1β, hippocampal BDNF, corticosterone, and glucose had significant correlations with hippocampal IL-1β levels. Conclusion: The synchronous alterations of some hippocampal factors, including BDNF, corticosterone, IL-1β, and glucose, caused by NBM lesion suggest that their interaction might play a significant role in neurodegeneration and relevant learning and memory impairments.
Highlights
The basal forebrain neurodegeneration results in learning and memory impairment
brain-derived neurotrophic factor (BDNF) decreased whereas corticosterone, glucose, and IL-1β levels increased in the hippocampus
The synchronous alterations of some hippocampal factors, including BDNF, corticosterone, IL-1β, and glucose, caused by nucleus basalis magnocellularis (NBM) lesion suggest that their interaction might play a significant role in neurodegeneration and relevant learning and memory impairments
Summary
The basal forebrain neurodegeneration results in learning and memory impairment. The basal forebrain cholinergic neurons along with the non-cholinergic ones are distributed in the medial septal nucleus, diagonal band nuclei, nucleus basalis, and substantia innominata. Several cholinergic fiber projections are sent to the amygdala, neocortex, and hippocampus.1. Many studies have emphasized the effects of diabetes mellitus, stress, and inflammation on the onset and progression of memory impairment. Only some of these conditions have been thoroughly investigated.[2,3,4] these studies did not connect these abnormalities with a primary pathogenic mechanism related to the cognitive impairments; instead, they have merely proposed various theories and focused on a specific pathological condition. The nucleus basalis magnocellularis (NBM) sends projections to the hippocampus that
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