Effect of Nucleus Basalis Magnocellularis Lesions on Memory and Hippocampal Brain-Derived Neurotrophic Factor, IL-1β, Glucose, and Corticosterone Levels in Adult Rats

Nasrin Hosseini, M. Radahmadi, H. Alaei, S. Nadjafi
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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.
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大鼠延髓基底核损伤对记忆和海马神经营养因子、IL-1β、葡萄糖和皮质酮水平的影响
背景:大细胞基底核(NBM)向海马发送与学习和记忆形成有关的投射。尽管有大量证据表明认知功能障碍与神经退行性变有关,但它可能是由生物化学物质的改变引起的。我们的目的是研究NBM病变对海马白介素-1β (IL-1β)、脑源性神经营养因子(BDNF)和皮质酮水平的影响,这些水平是炎症标志物,也是神经变性、应激和代谢状态的标志。方法:36只雄性Wistar大鼠随机分为对照组、假手术组和nbm损伤组。大鼠脑内注射10 μg伊博腾酸(5 μg/μL,每侧)诱导损伤后,采用被动回避试验评估记忆。此外,42天后测定血清和海马IL-1β水平,以及海马皮质酮、BDNF和葡萄糖水平。结果:nbm损伤组在不同时间间隔内保持力明显受损。海马区BDNF降低,皮质酮、葡萄糖和IL-1β水平升高。此外,血清IL-1β、海马BDNF、皮质酮和葡萄糖水平与海马IL-1β水平有显著相关性。结论:NBM病变引起的海马BDNF、皮质酮、IL-1β、葡萄糖等因子的同步改变提示它们的相互作用可能在神经退行性变及相关的学习记忆障碍中起重要作用。
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