Authors: Denis Larrivee.
The SHY proposal, which posits that sensorial input asymptotically leads to a limiting level of synaptic potentiation thus constraining neuroplastic learning, reflects a corollary thesis expressed by the free energy principle. This latter hypothesis claims that ongoing sensorial flow leads to a saturable rise in the information related, state variable, entropy, paralleling the claim advanced by the SHY proposal. Sleep, accordingly, is regarded as a homeostatic system essential for overcoming intrinsic thermodynamic constraints to optimize learning. Consistent with the circumvention of neuroplastic potentiation during sleep, subcortical nuclei have evolved mechanisms for extensive cortical influences that a) regulate sensorial input, b) globally synchronize neuroplastic recovery, c) initiate synaptic renormalization, and d) optimize learned and learning capacity. Among key nuclei involved in modulating NREM cortical activity are the thalamic reticular nucleus (TRN) and the centromedian nuclei. Cell intrinsic and cell microcircuit neural activity within these nuclei modulate the slow oscillation, a synchronized wave pervasive throughout the neocortex during NREM sleep, thereby promoting UP state initiation via gated non-sensory input and enhancing brain wide, slow wave synchrony, respectively. Slow wave nested, action potential bursting, driven by Ca2+ spiking, results in the opening of low-voltage-gated T-type Ca2+ channels (T-VGCCs) that appear to drive synaptic rescaling, while nested bursting in delta oscillatory activity may preserve neuroplastic learning. The possibility of bimodal synaptic modulation supports a dual behavioral role that is apparently grounded in an underlying drive to maximize learning efficiency.
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