Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

https://www.zora.uzh.ch/id/eprint/77770/1/physiol_rev_93.pdf

About sleep's role in memory

Reductions in blood flow to the brain of sufficient duration and extent lead to stroke, which results in damage to neuronal networks and the impairment of sensation, movement or cognition. Evidence from animal models suggests that a time-limited window of neuroplasticity opens following a stroke, during which the greatest gains in recovery occur. Plasticity mechanisms include activity-dependent rewiring and synapse strengthening. The challenge for improving stroke recovery is to understand how to optimally engage and modify surviving neuronal networks, to provide new response strategies that compensate for tissue lost to injury.

Plasticity during stroke recovery: from synapse to behaviour.

Our understanding of the cellular implementation of systems-level neural processes like action, thought and emotion has been limited by the availability of tools to interrogate specific classes of neural cells within intact, living brain tissue. Here we identify and develop an archaeal light-driven chloride pump (NpHR) from Natronomonas pharaonis for temporally precise optical inhibition of neural activity. NpHR allows either knockout of single action potentials, or sustained blockade of spiking. NpHR is compatible with ChR2, the previous optical excitation technology we have described, in that the two opposing probes operate at similar light powers but with well-separated action spectra. NpHR, like ChR2, functions in mammals without exogenous cofactors, and the two probes can be integrated with calcium imaging in mammalian brain tissue for bidirectional optical modulation and readout of neural activity. Likewise, NpHR and ChR2 can be targeted together to Caenorhabditis elegans muscle and cholinergic motor neurons to control locomotion bidirectionally. NpHR and ChR2 form a complete system for multimodal, high-speed, genetically targeted, all-optical interrogation of living neural circuits.

Multimodal fast optical interrogation of neural circuitry

http://neuroidss.ru/sites/default/files/nihms455900.pdf

The theta-gamma neural code

Grouping of brain rhythms in corticothalamic systems

To investigate synaptic events underlying sensory perception, we made whole-cell membrane potential recordings of barrel cortex neurons in awake mice while recording whisker-related behavior. During quiet periods, we recorded slow, large-amplitude membrane potential changes, which switched during whisking to small, fast fluctuations that were correlated with whisker position. Robust subthreshold responses were evoked by passive whisker stimulation during quiet behavior and by active whisker contact with an object.

Correlating whisker behavior with membrane potential in barrel cortex of awake mice

We investigated the impact of thalamus on ongoing cortical activity in the awake, behaving mouse. We demonstrate that the desynchronized cortical state during active behavior is driven by a centrally generated increase in thalamic action potential firing, which can also be mimicked by optogenetic stimulation of the thalamus. The thalamus therefore is key in controlling cortical states.

Thalamic control of cortical states.

https://www.cell.com/neuron/pdf/S0896-6273(11)00120-6.pdf

Synaptic Mechanisms Underlying Sparse Coding of Active Touch

https://www.cell.com/trends/pharmacological-sciences/pdf/S0165-6147(04)00281-0.pdf

The histamine H3 receptor as a novel therapeutic target for cognitive and sleep disorders

https://www.cell.com/neuron/pdf/S0896-6273(13)00267-5.pdf

Sylvain Crochet

Papers

Correlating whisker behavior with membrane potential in barrel cortex of awake mice

Thalamic control of cortical states.

Synaptic Mechanisms Underlying Sparse Coding of Active Touch

The histamine H3 receptor as a novel therapeutic target for cognitive and sleep disorders

Synaptic Computation and Sensory Processing in Neocortical Layer 2/3