论文部分内容阅读
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。BD-NF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 a molecular phenomenon in learning and memory. Many factors involved in the mechanism of LTP, recent studies have found that neurotrophic factors, especially brain-derived neurotrophic factor (BDNF) which plays an important regulatory role on LTP, but also for short-term and long-term synaptic plasticity influences. Functions that have been identified as neurotrophic factors include regulation of neural differentiation, growth and repair of neuronal axons and dendrites, and synapse formation. This article reviews the experimental evidence of the association between BDNF and LTP. It is concluded that BDNF influences the priming and maintenance of LTP through presynaptic and postsynaptic mechanisms. The direct mechanism of action of BD-NF is acting on the receptor on the synaptic membrane, resulting in increased presynaptic vesicles and increased neurotransmitter release. After the postsynaptic synapses cause postsynaptic membrane depolarization, which opens the voltage-dependent calcium channels, calcium concentration increased, eventually leading to an increase in the number of AMPA receptors, enhanced function, resulting in LTP.