| 研究実績の概要 |
Mammalian sleep is composed of rapid eye movement (REM) sleep and non-REM (NREM) sleep, both of which can be compromised differentially in various psychiatric and neurological disorders. I recently found that ablation of a specific neuronal population in the sublaterodorsal nucleus (SLD) resulted in significant loss of REM sleep, suggesting a genetically defined neuronal population is discovered to be essential for generating REM sleep. In the SLD neuron-ablated mice, REM sleep without muscle atonia is frequently observed, reminiscent of REM sleep behavior disorder in Parkinson's disease (PD). Moreover, lower anxiety-like and lower depression-like behaviors are found, consistent with previous observations in which REM sleep deprivation produced anxiolytic-like and antidepressant-like effect. Next, I found that the ablated neuronal population are composed of both GABAergic and glutamatergic neurons with varied percentages. Therefore, these results provide us more information about the pathogenesis of PD, during which the alpha-synuclein accumulation may occur in the level of the SLD, producing various motor and non-motor symptoms. Furthermore, the genetic identification of SLD neurons may lead to the development of novel diagnostic methods and therapeutics for PD.
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