Sleep deprivation and sleep recovery modifies connexin36 and connexin43 protein levels in rat brain.
Summary of "Sleep deprivation and sleep recovery modifies connexin36 and connexin43 protein levels in rat brain."
Gap junctional communication is mainly mediated by connexin36 and connexin43 in neurons and astrocytes, respectively. It has been suggested that connexin36 allows electrical coupling between neurons whereas connexin43 participates in several process including release of ATP. It was recently reported that blockage of gap junctional communication mediated by connexin36 can disrupt the sleep architecture of the rat. However, there is no experimental approach about effects of sleep deprivation on connexins expression. Therefore, we examined in adult male Wistar rats whether protein levels of connexin36 and connexin43 change in pons, hypothalamus, and frontal cortex after 24 h of total sleep deprivation and 4 h of sleep recovery. Western blot revealed that total sleep deprivation significantly decreases the levels of connexin36 in the hypothalamus and this decrease maintains after sleep recovery. Meanwhile, connexin43 is not altered by total sleep deprivation but interestingly the sleep recovery period induces an increase of this connexin. These results suggest that electrical coupling between hypothalamic neurons could be altered by sleep deprivation and that sleep recovery drives changes in connexin43 expression probably as a mechanism related to ATP release and energy regulation during sleep.
aDepartment of Neurophysiology bMedical Physics Laboratory, National Institute of Neurology and Neurosurgery cDepartment of Experimental Medicine, National Autonomous University of Mexico dMedical Proteomics Unit, National Institute of Genomic Medicine, M
This article was published in the following journal.
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22158029
- DOI: http://dx.doi.org/10.1097/WNR.0b013e32834e8fcb
Medical and Biotech [MESH] Definitions
Periods of sleep manifested by changes in EEG activity and certain behavioral correlates; includes Stage 1: sleep onset, drowsy sleep; Stage 2: light sleep; Stages 3 and 4: delta sleep, light sleep, deep sleep, telencephalic sleep.
The state of being deprived of sleep under experimental conditions, due to life events, or from a wide variety of pathophysiologic causes such as medication effect, chronic illness, psychiatric illness, or sleep disorder.
Sleep Disorders, Intrinsic
Dyssomnias (i.e., insomnias or hypersomnias) associated with dysfunction of internal sleep mechanisms or secondary to a sleep-related medical disorder (e.g., sleep apnea, post-traumatic sleep disorders, etc.). (From Thorpy, Sleep Disorders Medicine, 1994, p187)
Movements or behaviors associated with sleep, sleep stages, or partial arousals from sleep that may impair sleep maintenance. Parasomnias are generally divided into four groups: arousal disorders, sleep-wake transition disorders, parasomnias of REM sleep, and nonspecific parasomnias. (From Thorpy, Sleep Disorders Medicine, 1994, p191)
A sleep disorder of central nervous system origin characterized by prolonged nocturnal sleep and periods of daytime drowsiness. Affected individuals experience difficulty with awakening in the morning and may have associated sleep drunkenness, automatic behaviors, and memory disturbances. This condition differs from narcolepsy in that daytime sleep periods are longer, there is no association with CATAPLEXY, and the multiple sleep latency onset test does not record sleep-onset rapid eye movement sleep. (From Chokroverty, Sleep Disorders Medicine, 1994, pp319-20; Psychiatry Clin Neurosci 1998 Apr:52(2):125-129)
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