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Stability of cortical synapses across sleep and wake

Sleep is widely believed to be an essential regulator of synaptic plasticity, but there is disagreement on whether it primarily enables correlation-based plasticity mechanisms such as long-term potentiation (LTP), or homeostatic forms of plasticity. Notably, it has been postulated that patterns of brain activity during sleep induce a widespread homeostatic downscaling of excitatory synaptic strengths across the brain. Here we use a combination of real-time sleep classification, ex vivo measurements of postsynaptic strength, and in vivo optogenetic monitoring of thalamocortical synapses in primary visual cortex (V1) to ask whether sleep and wake states can constitutively drive synaptic plasticity within neocortical circuits. We found that miniature EPSCs onto L4 or L2/3 pyramidal neurons were stable across sleep and wake dense epochs in both V1 and prefrontal cortex (PFC). Further, chronic monitoring of thalamocortical synaptic efficacy in V1 of freely behaving animals revealed remarkable stability of thalamocortical transmission across prolonged natural sleep and wake epochs. Together these data provide strong evidence against the view that sleep drives widespread constitutive weakening of excitatory synaptic strengths.