Sleep Promotes Downward Firing Rate Homeostasis.
Sleep Promotes Downward Firing Rate Homeostasis.
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DOI：
10.1016/j.neuron.2020.11.001
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发表时间：
2021-02-03
期刊：
影响因子：
16.2
通讯作者：
Turrigiano GG
中科院分区：
文献类型：
--
作者：
Torrado Pacheco A;Bottorff J;Gao Y;Turrigiano GG
稳态可塑性被假设为双向调节神经元的活动在一个稳定的设定点，以补偿学习相关的可塑性，但迄今为止，只有向上放电率稳态（FRH）已被证明在体内。我们将自由行为动物的慢性电生理学与眼睛重新睁开范例相结合，以增强初级视觉皮层（V1）的放电，并发现神经元围绕单个设定点双向调节放电率。向下的FRH不需要N-甲基-D-天冬氨酸受体（NMDAR）信号传导，并与突触强度的稳态缩小有关。与向上的FRH一样，向下的FRH也受唤醒状态的门控，但方向相反：它发生在睡眠期间，而不是清醒期间。相反，与赫布可塑性相关的放电率抑制独立于睡眠和觉醒发生。因此，睡眠和清醒状态在时间上分离向上和向下的FRH，这可以防止干扰或在最需要时提供无对抗的稳态补偿。Torrado帕切科等人表明，在任何方向的活动扰动后，神经元都会围绕单个设定点调节其放电。向下的稳态调节仅限于睡眠，而向上的稳态调节仅发生在清醒时。唤醒状态的这种隔离可能会优化大脑可塑性机制之间的合作。
Homeostatic plasticity is hypothesized to bidirectionally regulate neuronal activity around a stable set point to compensate for learning-related plasticity, but to date only upward firing rate homeostasis (FRH) has been demonstrated in vivo. We combined chronic electrophysiology in freely behaving animals with an eye-reopening paradigm to enhance firing in primary visual cortex (V1) and found that neurons bidirectionally regulate firing rates around an individual set point. Downward FRH did not require N-methyl-D-aspartate receptor (NMDAR) signaling and was associated with homeostatic scaling down of synaptic strengths. Like upward FRH, downward FRH was gated by arousal state but in the opposite direction: it occurred during sleep, not during wake. In contrast, firing rate depression associated with Hebbian plasticity happened independently of sleep and wake. Thus, sleep and wake states temporally segregate upward and downward FRH, which might prevent interference or provide unopposed homeostatic compensation when it is needed most. Torrado Pacheco et al. show that neurons regulate their firing around an individual set point following perturbations of activity in either direction. Downward homeostatic regulation is restricted to sleep, whereas upward homeostatic regulation only occurs during wake. This segregation by arousal state may optimize cooperation among brain plasticity mechanisms.
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