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Possible Mechanisms for Impairments to Learning, Memory, and Attention due to Sleep Deprivation

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We suggest here that impairments to learning, memory, and attention following sleep deprivation are based on the following changes to the composition of neuromodulators and intracellular processes, affecting synaptic plasticity and the functioning of the hippocampal formation, as well as cortex-basal ganglia-thalamus-cortex circuits. Firstly, the Ca2+ concentration and expression of NMDA receptors decrease, preventing potentiation of the efficiency of synaptic transmission in the cortex and hippocampus. Secondly, the orexin concentration decreases, also degrading conditions for potentiation and weakening the transmission of excitation in the trisynaptic pathway via the hippocampus. The formation of neural representations of “object–place” associations deteriorates. Thirdly, the dopamine concentration decreases, though the adenosine level and the number of A1 receptors in the striatum increase, degrading the functioning of the cortex-basal ganglia-thalamus-cortex circuit. This weakens voluntary and involuntary attention, degrades the processing of sensory information, and impairs motor responses. Neuron excitation in the reinforcement circuits also decreases, weakening the motivational significance of stimuli.

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Correspondence to I. G. Sil’kis.

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Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 98, No. 10, pp. 1200–1212, October, 2012.

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Sil’kis, I.G. Possible Mechanisms for Impairments to Learning, Memory, and Attention due to Sleep Deprivation. Neurosci Behav Physi 44, 576–583 (2014). https://doi.org/10.1007/s11055-014-9954-x

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