Colbran Roger J
From the Department of Molecular Physiology & Biophysics, The Vanderbilt Brain Institute, and The Vanderbilt Kennedy Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232
J Biol Chem. 2015 Nov 27;290(48):28594-5. doi: 10.1074/jbc.R115.696468. Epub 2015 Oct 9.
The human brain contains ~86 billion neurons, which are precisely organized in specific brain regions and nuclei. High fidelity synaptic communication between subsets of neurons in specific circuits is required for most human behaviors, and is often disrupted in neuropsychiatric disorders. The presynaptic axon terminals of one neuron release neurotransmitters that activate receptors on multiple postsynaptic neuron targets to induce electrical and chemical responses. Typically, postsynaptic neurons integrate signals from multiple presynaptic neurons at thousands of synaptic inputs to control downstream communication to the next neuron in the circuit. Importantly, the strength (or efficiency) of signal transmission at each synapse can be modulated on time scales ranging up to the lifetime of the organism. This "synaptic plasticity" leads to changes in overall neuronal circuit activity, resulting in behavioral modifications. This series of minireviews will focus on recent advances in our understanding of the molecular and cellular mechanisms that control synaptic plasticity.
人类大脑包含约860亿个神经元,这些神经元精确地组织在特定的脑区和神经核中。特定神经回路中神经元子集之间的高保真突触通讯是大多数人类行为所必需的,并且在神经精神疾病中常常受到破坏。一个神经元的突触前轴突末端释放神经递质,这些神经递质激活多个突触后神经元靶标的受体,以诱导电反应和化学反应。通常,突触后神经元在数千个突触输入处整合来自多个突触前神经元的信号,以控制向回路中下一个神经元的下游通讯。重要的是,每个突触处信号传递的强度(或效率)可以在长达生物体寿命的时间尺度上进行调节。这种“突触可塑性”导致整体神经元回路活动的变化,从而引起行为改变。本系列小型综述将聚焦于我们对控制突触可塑性的分子和细胞机制的最新认识进展。