Sleep is a fundamental, conserved biological process, yet the essential physiological function of sleep remains an open question. Accumulating evidence supports a role for sleep in memory consolidation and maintenance of cognitive function. However, the neural substrates of and mechanisms underlying sleep-facilitated memory consolidation remain poorly understood.
One prominent hypothesis suggests that during sleep, ensemble patterns of neuronal activity which occurred during awake experience are reactivated to induce or consolidate synaptic plasticity, thus consolidating experience-relevant synaptic changes into long-lasting plasticity and memory.
An alternative hypothesis posits that sleep is a critical homeostatic process. This synaptic homeostasis hypothesis is based on observations that synaptic strength generally increases during waking periods and decreases during sleep. This ebb and flow suggests that progressive increases in synaptic strength accumulate in response to awake experience, and that downscaling of synaptic strength during sleep is a restorative process necessary to maintain neuronal firing rates at a level conducive to continued information processing.
While these two hypotheses are apparently contradictory, they are not mutually exclusive: it is possible that sleep facilitates a more complicated information triage in which neuronal representations of salient experience are strengthened amidst more global homeostatic downscaling of less important information.
We are using genetic tools to label and manipulate neuronal populations that participate in reactivation during sleep in order to investigate the synaptic changes induced by selective neuronal reactivation versus global downscaling in sleep, and to determine which of these changes are necessary for memory consolidation and maintenance of cognition.