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Curr Opin Neurobiol. 2017 Jun;44:202-211. doi: 10.1016/j.conb.2017.05.002. Epub 2017 May 30.

Sleep homeostasis, habits and habituation.

Author information

1
Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, United Kingdom; Sleep and Circadian Neuroscience Institute, Oxford Molecular Pathology Institute, Sir William Dunn School of Pathology, South Parks Road, Oxford OX1 3RE, United Kingdom. Electronic address: vladyslav.vyazovskiy@dpag.ox.ac.uk.
2
Department of Experimental Psychology, University of Oxford,South Parks Road, Oxford OX1 3UD, United Kingdom.
3
Sleep and Circadian Neuroscience Institute, Oxford Molecular Pathology Institute, Sir William Dunn School of Pathology, South Parks Road, Oxford OX1 3RE, United Kingdom.
4
Sleep and Circadian Neuroscience Institute, Oxford Molecular Pathology Institute, Sir William Dunn School of Pathology, South Parks Road, Oxford OX1 3RE, United Kingdom; Department of Experimental Psychology, University of Oxford,South Parks Road, Oxford OX1 3UD, United Kingdom.

Abstract

The importance of sleep for behavioural performance during waking is long-established, but the underlying reasons and mechanisms remain elusive. Waking and sleep are associated with changes in the levels of GluA1 AMPAR subunit in synaptic membranes, while studies using genetically-modified mice have identified an important role for GluA1-dependent synaptic plasticity in a non-associative form of memory that underlies short-term habituation to recently experienced stimuli. Here we posit that sleep may play a role in dishabituation, which restores attentional capacity and maximises the readiness of the animal for learning and goal-directed behaviour during subsequent wakefulness. Furthermore we suggest that sleep disturbance may fundamentally change the nature of behaviour, making it more model-free and habitual as a result of reduced attentional capacity.

PMID:
28575718
DOI:
10.1016/j.conb.2017.05.002
[Indexed for MEDLINE]
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