It is commonly accepted that brain plasticity occurs in wakefulness sleep. However, how these different brain states work in concert to create long-lasting changes in brain circuitry is unclear. Considering that wakefulness and sleep are profoundly different brain states on multiple levels (e.g., cellular, molecular and network activation), it is unlikely that they operate exactly the same way. Rather it is probable that they engage different, but coordinated, mechanisms. In this article we discuss how plasticity may be divided across the sleep-wake cycle, and how synaptic changes in each brain state are linked. Our working model proposes that waking experience triggers short-lived synaptic events that are necessary for transient plastic changes and mark (i.e., 'prime') circuits and synapses for further processing in sleep. During sleep, synaptic protein synthesis at primed synapses leads to structural changes necessary for long-term information storage.
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http://dx.doi.org/10.3389/fnsys.2019.00002 | DOI Listing |
Expert Opin Drug Deliv
January 2025
CICS-UBI - Health Sciences Research Centre, University of Beira Interior, Covilhã, Portugal.
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Department of Kinesiology, Michigan State University, 308 W Circle Dr, East Lansing, USA.
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View Article and Find Full Text PDFActa Neuropathol
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Department of Neurology, NYU Grossman School of Medicine, New York, NY, USA.
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Department of Physics and Astronomy, The University of Tennessee, Knoxville, Tennessee 37996, United States.
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Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.
The neurobiological mechanisms driving the ictal-interictal fluctuations and the chronification of migraine remain elusive. We aimed to construct a composite genetic-microRNA model that could reflect the dynamic perturbations of the disease course and inform the pathogenesis of migraine. We prospectively recruited four groups of participants, including interictal episodic migraine (i.
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