Synapse-specific control of synaptic efficacy at the terminals of a single neuron
Synapse-specific control of synaptic efficacy at the terminals of a single neuron
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DOI：
10.1038/32176
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发表时间：
1998-03-05
期刊：
影响因子：
64.8
通讯作者：
Goodman, CS
中科院分区：
文献类型：
--
作者：
Davis, GW;Goodman, CS
突触效能的调节对于神经回路的正常功能是必不可少的。如果突触增益设置得过高或过低，细胞要么被不适当地激活，要么保持沉默。存在额外的复杂性，因为突触不是静态的，而是在整个生命过程中形成，收缩，扩张，加强和减弱，控制突触功效的稳态调节机制可能存在，以确保神经元在有意义的生理范围内保持功能（1-5）。用于分析调节突触功效的机制的最好定义的系统之一是神经肌肉接头。在从昆虫到人类的生物体中，研究表明，突触功效的变化与发育过程中肌肉大小的变化紧密相关（1，6 -8）。有人提出，从肌肉到运动神经元的信号保持这种耦合（9）。在这里，我们表明，通过基因操纵肌肉神经支配，有两个独立的机制，肌肉调节突触的功效在终端的单个运动神经元。增加的肌肉神经支配导致突触前递质释放的代偿性、靶特异性减少，这意味着突触前释放的逆行调节。减少的肌肉神经支配导致量子大小的代偿性增加。
The regulation of synaptic efficacy is essential for the proper functioning of neural circuits, If synaptic gain is set too high or too low cells are either activated inappropriately or remain silent. There is extra complexity because synapses are not static, but form, retract, expand, strengthen, and weaken throughout life, Homeostatic regulatory mechanisms that control synaptic efficacy presumably exist to ensure that neurons remain functional within a meaningful physiological range(1-5). One of the best defined systems for analysis of the mechanisms that regulate synaptic efficacy is the neuromuscular junction. It has been shown, in organisms ranging from insects to humans, that changes in synaptic efficacy are tightly coupled to changes in muscle size during development(1,6-8). It has been proposed that a signal from muscle to motor neuron maintains this coupling(9). Here we show, by genetically manipulating muscle innervation, that there are two independent mechanisms by which muscle regulates synaptic efficacy at the terminals of single motor neurons. Increased muscle innervation results in a compensatory, target-specific decrease in presynaptic transmitter release, implying a retrograde regulation of presynaptic release, Decreased muscle innervation results in a compensatory increase in quantal size.