Neural systems use homeostatic plasticity to maintain normal brain functions and to prevent abnormal activity. Surprisingly, homeostatic mechanisms that regulate circuit output have mainly been demonstrated during artificial and/or pathological perturbations. Natural, physiological scenarios that activate these stabilizing mechanisms in neural networks of mature animals remain elusive. To establish the extent to which a naturally inactive circuit engages mechanisms of homeostatic plasticity, we utilized the respiratory motor circuit in bullfrogs that normally remains inactive for several months during the winter. We found that inactive respiratory motoneurons exhibit a classic form of homeostatic plasticity, up-scaling of AMPA-glutamate receptors. Up-scaling increased the synaptic strength of respiratory motoneurons and acted to boost motor amplitude from the respiratory network following months of inactivity. Our results show that synaptic scaling sustains strength of the respiratory motor output following months of inactivity, thereby supporting a major neuroscience hypothesis in a normal context for an adult animal.

中文翻译：

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突触放大可在慢性自然不活动后保留运动电路输出

神经系统使用稳态可塑性来维持正常的大脑功能并防止异常活动。令人惊讶的是，调节电路输出的稳态机制主要在人工和/或病理扰动期间得到证实。在成熟动物的神经网络中激活这些稳定机制的自然生理场景仍然难以捉摸。为了确定自然不活跃的回路在多大程度上参与稳态可塑性机制，我们利用了牛蛙的呼吸运动回路，牛蛙在冬天通常会保持几个月不活跃。我们发现不活动的呼吸运动神经元表现出经典形式的稳态可塑性，AMPA-谷氨酸受体的放大。放大增加了呼吸运动神经元的突触强度，并在数月不活动后提高了呼吸网络的运动幅度。我们的结果表明，突触缩放在数月不活动后维持呼吸运动输出的强度，从而支持成年动物正常情况下的主要神经科学假设。