Compensatory increase in sleep is a novel therapeutic application for depression

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K15463
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pharmacology in pharmacy
• Research Institution: Fukuoka University
• Principal Investigator: Murata Yusuke 福岡大学, 薬学部, 助教 (90461508)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 過眠 / 睡眠不足 / 断眠処置 / 海馬 / BDNF / グルタミン酸受容体 / neurotensin

Outline of Final Research Achievements

Sleep loss-induced increase in sleep is considered as an innate recovery system, however, the molecular mechanisms remain unclear. Male rats were subjected to sleep deprivation for 96-h, then returned to a normal housing condition for taking a sleep freely. Six hours, 3- or 7-days after, animals were sacrificed and hippocampal tissues were collected in order to quantify various gene transcripts using RT-qPCR. We found three major findings: 1) rebound sleep increased splicing variants levels of brain derived neurotrophic factor gene, 2) the glutamate receptor gene transcripts levels were incresed or decreased by rebound sleep dependent of subtypes, 3) the decrease in neurotensin mRNA levels immediately after rebound sleep was increased gradiently over the baseline. These findings suggest that the compensentory increased sleep may ameliorate sleep loss-induced damages of neuronal functions via complex and multifactorial processes.

Free Research Field

精神神経薬理学

Academic Significance and Societal Importance of the Research Achievements

本研究は、睡眠不足後に誘発される「過眠」は、確かに脳内に蓄積した損傷を回復させるという一般的理解について、分子生理学的メカニズムの観点から支持するものである。また「過眠」による回復と海馬neurotensinの間の関連が初めて明らかとなった。
これらの成果より、「睡眠不足によるダメージの回復には、やはり十分な睡眠が必要」という厳然たる事実が保証された。またneurotensinを標的とした「過眠模倣物質」、言い換えると「実際に睡眠時間の増加がなくても睡眠を十分に取ったかのような回復反応を促す物質」の創出が期待される。