Sleep promotes downward firing rate homeostasis

Homeostatic plasticity is hypothesized to regulate neuronal activity around a stable set point to compensate for learning-related plasticity. This regulation is predicted to be bidirectional but only upward firing rate homeostasis (FRH) has been demonstrated in vivo. We combined chronic electrophysiology in freely behaving animals with a protocol that induces robust plasticity in primary visual cortex (V1) to induce downward FRH and show 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 vigilance state, but in the opposite direction: it occurred during sleep and not during wake. In contrast, FR changes associated with Hebbian plasticity happened independently of sleep and wake. Thus, we find that sleeps impact on neuronal plasticity depends on the particular forms of plasticity that are engaged.