脑源性神经营养因子的概述及其对海马兴奋毒性易感性的影响。

International Journal of Peptides Pub Date : 2011-01-01 Epub Date: 2011-09-28 DOI:10.1155/2011/654085
Patrick S Murray, Philip V Holmes
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引用次数: 128

摘要

本文探讨了脑源性神经营养因子(BDNF)在海马形成中的性质和功能及其表达变化的后果。本文重点介绍了BDNF在海马发育和神经可塑性中的作用。BDNF的表达对发育和环境因素高度敏感,BDNF信号的增加促进了神经发生、神经突发芽、电生理活动和其他反映海马功能普遍增强的过程。这种活动的增加可能会带来一些有益的影响,比如学习和记忆的增强。然而,活动的增加也是有代价的:BDNF的可塑性使海马体更容易受到过度兴奋性和/或兴奋性毒性损伤。运动显著增加海马BDNF水平,并产生与此现象一致的行为效应。通过分析有关运动诱导BDNF调节的文献,本文为BDNF可塑性的潜在有害后果如何被其他内源性因素调节提供了一个理论模型。肽丙氨酸可能通过调节海马的兴奋性来发挥这样的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

An overview of brain-derived neurotrophic factor and implications for excitotoxic vulnerability in the hippocampus.

An overview of brain-derived neurotrophic factor and implications for excitotoxic vulnerability in the hippocampus.

An overview of brain-derived neurotrophic factor and implications for excitotoxic vulnerability in the hippocampus.

An overview of brain-derived neurotrophic factor and implications for excitotoxic vulnerability in the hippocampus.

The present paper examines the nature and function of brain-derived neurotrophic factor (BDNF) in the hippocampal formation and the consequences of changes in its expression. The paper focuses on literature describing the role of BDNF in hippocampal development and neuroplasticity. BDNF expression is highly sensitive to developmental and environmental factors, and increased BDNF signaling enhances neurogenesis, neurite sprouting, electrophysiological activity, and other processes reflective of a general enhancement of hippocampal function. Such increases in activity may mediate beneficial effects such as enhanced learning and memory. However, the increased activity also comes at a cost: BDNF plasticity renders the hippocampus more vulnerable to hyperexcitability and/or excitotoxic damage. Exercise dramatically increases hippocampal BDNF levels and produces behavioral effects consistent with this phenomenon. In analyzing the literature regarding exercise-induced regulation of BDNF, this paper provides a theoretical model for how the potentially deleterious consequences of BDNF plasticity may be modulated by other endogenous factors. The peptide galanin may play such a role by regulating hippocampal excitability.

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