Sleep promotes downward firing rate homeostasis

Abstract

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 observed 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 FRs are bidirectionally regulated around a cell-autonomous set point. Downward FRH did not require Nmethyl-D-aspartate receptor (NMDAR) function 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 sleep's impact on neuronal plasticity depends on the particular mechanisms of synaptic plasticity that are engaged.

CaMKIV Signaling Is Not Essential for the Maintenance of Intrinsic or Synaptic Properties in Mouse Visual Cortex

“…The function of CaMKIV signaling in cultured neurons may also be distinct from its function in vivo in L2/3 or L4. Firing rate set points are homeostatically maintained at the single neuron level in vivo (Dhawale et al, 2017;Hengen et al, 2016;Pacheco et al, 2021), but at the network level in cultured neurons (Slomowitz et al, 2015;Styr et al, 2019), which lack the stereotypical layered structure of intact cortex. This suggests that the specific connectivity of neurons may be critical for their expression of homeostatic plasticity.…”

Homeostatic Synaptic Scaling Establishes the Specificity of an Associative Memory

“…2g). To test whether mEPSC amplitude increased multiplicatively, as is characteristic of synaptic scaling 11 , we plotted ranked inhibited vs. ranked control amplitudes and fit a linear function to the data 11,32 ; scaling the inhibited distribution down generated a distribution that was statistically indistinguishable from the control (Fig. 2g).…”

“…The pAAV-CMV-GluA2-CT (GluA2-Ctail) and pAAV-CMV-PSD95-PDZ1/2 (PSD-PDZ1/2) plasmids were constructed by sub-cloning the coding sequences of the scaling blockers 32,35 into the pAAV-CMV-eGFP3 vector (Empty Vector). pAAV-RAM-dtTA-TRE-tdTomato was constructed by replacing GFP in pAAV-RAM-dtTA-TRE-GFP (Addgene: 84469) with the coding sequence of tdTomato.…”

Psilocin acutely disrupts sleep and affects local but not global sleep homeostasis in laboratory mice

“…Neuronal plasticity processes, at both structural and functional levels, whether adaptive or homeostatic, are shaped by ongoing neuronal activity. Importantly, the brain-wide changes in neuronal dynamics which occur in association with the sleep-wake cycle are strongly implicated in the regulation of plasticity of cortical function; for example, cellular maintenance, synaptic scaling, firing rate homeostasis and systems-level memory consolidation are enabled by the sleep state (Vyazovskiy & Harris, 2013; Rasch & Born, 2013; Tononi & Cirelli, 2014; Watson et al, 2016; Levenstein et al, 2017; Pacheco et al, 2020). Alongside the circadian rhythm, the occurrence of sleep is itself regulated by a homeostatic principle; prolonged wakefulness is compensated for by increased sleep intensity, enabling an approximately constant sleep quantity to be obtained each day (Borbély et al, 2016).…”