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首页> 外文期刊>Nature >Synapse-specific control of synaptic efficacy at the terminals of a single neuron.
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Synapse-specific control of synaptic efficacy at the terminals of a single neuron.

机译：在单个神经元末端的突触特异性控制突触功效。

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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. 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. It has been proposed that a signal from muscle to motor neuron maintains this coupling. 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.
机译：突触功效的调节对于神经回路的正常运转至关重要。如果突触增益设置得太高或太低，细胞要么激活不当，要么保持沉默。因为突触不是一成不变的，而是在整个生命中形成，缩回，扩展，加强和减弱的，所以存在额外的复杂性。大概存在控制突触功效的稳态调节机制，以确保神经元在有意义的生理范围内保持功能。用于调节突触功效的机制的最佳定义系统之一是神经肌肉接头。已经表明，在从昆虫到人类的生物中，突触效力的变化与发育过程中肌肉大小的变化紧密相关。已经提出，从肌肉到运动神经元的信号保持这种耦合。在这里，我们通过遗传操纵肌肉神经支配来显示，有两种独立的机制，肌肉可以通过这种机制来调节单个运动神经元末端的突触功效。增强的肌肉神经支配导致突触前递质释放的代偿性，靶标特异性降低，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数量大小的补偿性增加。

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