Affiliations: [a] Laboratory of Functional Neuroscience, Spanish Network of Excellence for Research on Neurodegenerative Diseases (CIBERNED), University Pablo de Olavide, Seville, Spain | [b] Area de Fisiologia, Facultad de Medicina, Universidad de Cadiz, Cadiz, Spain | [c] Centro de Biologia Molecular “Severo Ochoa” (CSIC-UAM), Spanish Network of Excellence for Research on Neurodegenerative Diseases (CIBERNED), Campus de Cantoblanco, Madrid, Spain
Correspondence:
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Correspondence to: Jose L. Cantero, Ph.D., Laboratory of Functional Neuroscience, University Pablo de Olavide, Ctra. de Utrera, Km. 1, 41013 Seville, Spain. E-mail: jlcanlor@upo.es.
Abstract: Evidence has shown that the lack of tau produces subtle changes in neuronal structure and modest impairment in complex behaviors, suggesting compensatory mechanisms carried out by other neuronal microtubule-associated proteins. Here we show major abnormalities in sleep-wake cycle of tau-deficient animals including increased wakefulness duration and decreased non-rapid eye movement (NREM) sleep time, a higher number of state transitions between NREM and wake, and shortened sleep bouts. Altered sleep structure in tau-/- mice was accompanied by a significant decline in delta power together with an enhanced spectral density of sleep spindles during NREM sleep. No significant differences were observed in rapid eye movement (REM) sleep between the two mouse strains. Taken together, these results suggest that tau indirectly participates in the regulation of the sleep-wake cycle modulating not only the control and maintenance of global brain states but also the cerebral oscillatory patterns underlying sleep-wake states.
Keywords: Animal models, local field potential, microtubule-associated proteins, neuronal cytoskeleton, sleep-wake regulation, state-dependent brain oscillations, tau
