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.
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DOI：
10.1155/2011/654085
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Holmes PV
中科院分区：
文献类型：
--
作者：
Murray PS;Holmes PV
本文探讨了脑源性神经营养因子（BDNF）在海马结构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表达对发育和环境因素高度敏感，并且增加的BDNF信号传导增强神经发生、神经突发芽、电生理活性和反映海马功能普遍增强的其他过程。这种活动的增加可以介导有益的效果，例如增强学习和记忆。然而，增加的活动也是有代价的：BDNF可塑性使海马更容易受到过度兴奋和/或兴奋性毒性损伤。运动显著增加海马BDNF水平，并产生与这种现象一致的行为效应。在分析有关运动诱导的BDNF调节的文献中，本文提供了一个理论模型，说明BDNF可塑性的潜在有害后果可能受到其他内源性因素的调节。甘丙肽可能通过调节海马的兴奋性发挥这种作用。
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.