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Kunath, N.

Publications and source records attributed to Kunath, N..

3 recordsLinked to original sources

Sustained polyphasic sleep restriction abolishes human growth hormone release

Voluntary sleep restriction is a common phenomenon in industrialized societies aiming to increase time spent awake and thus productivity. We explored how restricting sleep to a radically polyphasic schedule affects neural, cognitive, and endocrine characteristics. Ten young healthy participants were restricted to one 30-min nap opportunity at the end of every 4 hours (i.e., 6 sleep episodes per 24 hours) without any extended core sleep window, which resulted in a cumulative sleep amount of just 2 hours per day (i.e., [~]20 min per bout). All but one participant terminated this schedule during the first three weeks. The remaining participant (a 25-year-old male) succeeded to adhere to a polyphasic schedule for 5 weeks with no apparent impairments in cognitive and psychiatric measures except for psychomotor vigilance. While in-blood cortisol or melatonin release pattern and amounts were unaltered by the polyphasic as compared to monophasic sleep, growth hormone seemed almost entirely abolished (>95% decrease), with the residual release showing a considerably changed polyphasic secretional pattern. While coarse sleep structure appeared intact during polyphasic sleep, REM sleep showed decreased oscillatory and increased aperiodic EEG activity compared to monophasic sleep. Considering the decreased vigilance, abolished growth hormone release, and neurophysiological changes observed, it is doubtful that radically polyphasic sleep schedules can subserve the different functions of sleep to a sufficient degree.

neuroscience↗

DNA repair enzyme NEIL3 enables a stable neural representation of space by shaping transcription in hippocampal neurons

DNA repair enzymes are essential for the maintenance of neuronal genome and thereby proper brain functions. NEIL3 is a member of the NEIL family DNA glycosylases initiating oxidative DNA base excision repair. Recent studies show that NEIL3-deficiency leads to impaired spatial performance in mice, decreased adult neurogenesis and altered synaptic composition in the hippocampus. However, it remains elusive how NEIL3 contributes to spatial information coding in hippocampal neurons. Here, we revealed impaired spatial stability in Neil3-/- CA1 place cells, demonstrating a functional interference of NEIL3 with spatial representations. We identified NEIL3-dependent transcriptional changes in response to spatial exploration and defined its regulatory role specifically for NMDA receptor subunits and immediate early genes. Our work demonstrates a non-canonical role of NEIL3 in modulating the functional plasticity of place cells by shaping the neuronal transcriptome, thus sheds light on the molecular determinants enabling a stable neural representation of space.

neuroscience↗

NEIL1 and NEIL2 DNA glycosylases regulate anxiety and learning in a cooperative manner

Oxidative DNA damage in the brain has been implicated in neurodegeneration and cognitive decline. DNA glycosylases initiate base excision repair (BER), the main pathway for oxidative DNA base lesion repair. NEIL1 and NEIL3 DNA glycosylases alter cognition in mice, the role of NEIL2 remains unclear. Here, we investigate the impact of NEIL2 and its potential overlap with NEIL1 on behavior in single and double knock-out mouse models. Neil1-/-Neil2-/- mice displayed hyperactivity, reduced anxiety and improved learning. Hippocampal oxidative DNA base lesion levels were comparable between genotypes, no mutator phenotype was found. Impaired canonical repair was thus not the cause of altered behavior. Electrophysiology indicated reduced stratum oriens afferents in the hippocampal CA1 region in Neil1-/-Neil2-/-. Within CA1, NEIL1 and NEIL2 jointly regulated transcription in genes relevant for synaptic function. Thus, we postulate a cooperative function of NEIL1 and NEIL2 in genome regulation beyond canonical BER modulating memory formation and anxiety.

molecular biology↗