Browsing by Subject "sleep deprivation"

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  • Rekola, Lauri (Helsingfors universitet, 2017)
    Despite decades of study, no ironclad conclusion has been reached concerning the biological function of sleep in humans. Recent theories have proposed that sleep might play a role in maintaining cortical excitability at safe levels by downregulating excessive intersynaptic connections accumulated during a waking episode. In line with this theory, sleep deprivation has been shown to increase cortical excitability in studies using transcranial magnetic stimulation (TMS) and electroencephalography (EEG). In this pilot study (N=4) we used magnetoencephalography (MEG) to study the effects of 24 hours of sleep deprivation on somatosensory evoked fields (SEFs). Sleep deprivation increased the amplitude of primary somatosensory P35m component by 36%. Our preliminary findings confirm and delineate the previous EEG findings of enhanced somatosensory activation after sleep deprivation, thus indicating increased cortical excitability following sleep loss.
  • Michalowski, Piotr (Helsingin yliopisto, 2019)
    The TrkB signaling pathway plays an important role in synaptic transmission and plasticity. Synaptic plasticity is disrupted in many neurological disorders, such as major depression and dementia. A number of studies indicate that TrkB (tropomyosin-related kinase B) signaling is required for the therapeutic effects of antidepressants. Both conventional and rapid-acting antidepressants encompass the TrkB pathway but the underlying mechanism of this remains unknown. Recent studies have, however, revealed an intriguing link between emergence of slow wave EEG activity (SWA) or sedation and the TrkB pathway. Notably, various anesthetics and sedatives (e.g. isoflurane and medetomidine) that increase SWA concomitantly induce TrkB signalling, and this seems to happen independently of BDNF (brain-derived neurotrophic factor), the primary ligand of TrkB. Given the ability of Src kinase to transactivate TrkB in vitro, we have examined the acute effects of medetomidine and isoflurane on SrcY416 and TrkBY816 phosphorylation in the adult rodent cortex and hippocampus by using Western blotting. Pyrazolopyrimidine 2 (PP2), a Src kinase inhibitor, was implemented in order to inhibit TrkB signalling pathway induced by medetomidine. The study was further extended to sleep deprivation experiments to investigate the effects of deep sleep on the Src and TrkB protein phosphorylation. Phosphorylation of GSK3βS9, another important molecular event coupled with antidepressant effects, was also investigated. The results indicate that both isoflurane and medetomidine activate Src kinase and TrkB signalling pathway. Such an effect was not, however, seen in the PP2 study and thus we failed to confirm the mechanistic connection between Src and TrkB. A trend in the phosphorylation of TrkB, Src and GSK3β was found in the brain samples collected after 15 minutes of recovery sleep, suggesting that TrkB signalling is also facilitated during physiological SWA. In conclusion, these results reinforce the hypothesis that SWA occurs simultaneously with TrkB signaling. Future studies are required to test the involvement of Src kinase in this phenomenon.