title: [Possible mechanisms of learning, memory and attention impairment in consequence of sleep deprivation].
abstract: We proposed that impairment of learning, memory, and attention evoked by sleep deprivation could be a consequence of following changes in neuromodulator concentrations and intracellular processes that influence synaptic plasticity and functioning of the hippocampal formation and cortico--basal ganglia--thalamocortical loops. Firstly, a decrease in Ca2+ concentration and NMDA-receptor expression prevents induction of LTP of efficacy of synaptic transmissions in the neocortex and hippocampus. Secondly, a decrease in orexin concentration also worsens conditions for LTP induction and suppresses transmission of excitation in trisynaptic pathway through the hippocampus, thus worsening a creation of neural representations of "object-place" associations. Thirdly, a decrease in concentration of dopamine, and increase in level of adenosine and number of A1 receptors in the striatum worsen the functioning ofcortico-basal ganglia-thalamocortical loops. These lead to decrease in voluntary and involuntary attention, worsens processing of sensory information, and motor reactions. Excitation of neurons in reinforcement loops is also decreased thus suppressing the motivational significance of stimuli.
authors: I G
authors: IG
authors: Sil'kis
mesh_terms: D001288:Attention / Q000502:physiology*; D001479:Basal Ganglia / Q000502:physiology; D002540:Cerebral Cortex / Q000502:physiology; D006624:Hippocampus / Q000502:physiology; D006801:Humans; D007858:Learning / Q000502:physiology*; D008568:Memory / Q000502:physiology*; D009473:Neuronal Plasticity; D009474:Neurons / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism / Q000502:physiology; D012892:Sleep Deprivation / Q000503:physiopathology; D013569:Synapses / Q000502:physiology*; D013788:Thalamus / Q000378:metabolism / Q000502:physiology
chemical_list: D016194:Receptors, N-Methyl-D-Aspartate