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.

假设稳态可塑性在稳定的设定点附近双向调节神经元活动，以补偿与学习相关的可塑性，但迄今为止，仅在体内证实了向上放电率稳态 (FRH). 我们将自由行为动物的慢性电生理学与睁眼模式相结合，以增强初级视觉皮层 (V1) 的放电，并发现神经元在单个设定点附近双向调节放电率。向下 FRH 不需要 N-甲基-D-天冬氨酸受体 (NMDAR) 信号传导，并且与突触强度的稳态缩小有关。与向上的 FRH 一样，向下的 FRH 由唤醒状态门控，但方向相反：它发生在睡眠期间，而不是在清醒期间。相比之下，与赫布可塑性相关的放电率降低独立于睡眠和清醒发生。因此，睡眠和唤醒状态在时间上将 FRH 向上和向下分离，这可以防止干扰或在最需要的时候提供无对抗的稳态补偿。