LTP研究进展(Ⅲ)——LTP和神经趋向因子

摘要

长时程增强(LTP)是学习和记忆过程的分子水平现象.参与LTP机制的因素很多,最近研究发现神经趋向因子,特别是其中的脑衍生的神经趋向因子(BDNF)对LTP起着重要的调节作用,而且对短时程及长时程突触可塑性均有影响.已经明确的神经趋向因子的功能包括调节神经分化,神经元轴突和树突的生长和修复,以及突触形成.本文综述了BDNF与LTP相关性的实验性根据.总结了BDNF通过突触前以及突触后机制影响LTP的引发和后期维持.BDNF的直接作用机制是作用于突触前后膜上的受体,导致突触前递质小泡增多从而增加递质释放.在突触后引起突触后膜去极化,从而打开电压依赖性钙通道、钙离子浓度增高,最终导致AMPA受体数目增多,功能强化,产生LTP.%Long-term potentiation (LTP) is believed underlined learning and memory. Recent research has attracted to brain-derived neurotrophic factor (BDNF) that may affect synaptic plasticity in both short- and long-term actions at the synapse. In vitro, neurotrophin regulate neuronal differentiation, axonal and dendritic growth and repair, synaptic formation, and synaptic plasticity. Here we summarized the experimental evidence linking BDNF to LTP. BDNF plays a role in LTP induction and late phase maintenance. The actions of BDNF are mediated by the TrkB receptor tyrosine kinase. BDNF potentiate LTP by modulating the number of docked vesicles and the level of vesicle protein on pre-synapse to increase neurotransmitter release, and by inducing postsynaptic depolarization to open voltage dependent Ca2+ channels. We also introduced the effects of LTP on the secretion of the neurotrophin. The experimental evidence strongly supports a role for BDNF in synaptic plasticity and should prompt further exploration of their functions at the synapse.