Development of REM sleep

快速眼动睡眠的发展

• 批准号: 7109153
• 负责人: David Sharpe Heister
• 金额: $ 3.09万
• 依托单位: UNIV OF ARKANSAS FOR MED SCIS
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-05-23 至 2010-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7109153
• 关键词: REM sleep; acetylcholine; anticholinergic agent; brain stem; cholinergic agents; developmental neurobiology; developmental psychology; electrophysiology; gap junctions; immunocytochemistry; ion channel blocker; laboratory rat; membrane channels; neurogenesis; neuropharmacology; pons; predoctoral investigator; reticular formation; sleep regulatory center; tegmentum; tissue /cell culture

DESCRIPTION (provided by applicant): The human infant sleeps 16 hrs/day, 8 as rapid eye movement (REM) sleep. The amount of REM sleep decreases dramatically from birth until puberty. Our overall hypothesis is that if this developmental decrease in REM sleep does NOT occur, a lifelong increase in REM sleep drive may ensue. Increased REM sleep drive is present in such disorders of hypervigilance as schizophrenia, anxiety disorder and depression, which have a predominantly developmental etiology. The main region controlling arousal and sleep is the reticular activating system (RAS), and the pedunculopontine nucleus (PPN), its cholinergic arm, helps generate REM sleep via its projections to various targets. One target, the SubCoeruleus nucleus (SubC), is known to manifest P-waves, paroxysmal wavefronts of activity thought to lead to the transition from slow wave sleep into REM sleep. The proposed studies will investigate the development of cholinergic input to the SubC, and the ability of the PPN to drive SubC cells during the developmental decrease in REM sleep in the rat, which occurs between 10 and 30 days postnatally. We hypothesize that P-waves may be facilitated by gap Junctions, a mechanism that will be studied for its potential to underlie pathology in this system.

描述（由申请人提供）：人类婴儿每天睡眠 16 小时，其中 8 小时为快速眼动 (REM) 睡眠。从出生到青春期，快速眼动睡眠时间急剧减少。我们的总体假设是，如果快速眼动睡眠的发育性下降没有发生，那么快速眼动睡眠驱动力的终生增加可能会随之而来。快速眼动睡眠驱动力增加存在于精神分裂症、焦虑症和抑郁症等过度警觉性疾病中，这些疾病的病因主要是发育性的。控制觉醒和睡眠的主要区域是网状激活系统 (RAS)，而桥脚核 (PPN) 是其胆碱能臂，通过投射到各种目标来帮助产生快速眼动睡眠。蓝核下核 (SubC) 是一个目标，已知它会表现出 P 波，即阵发性波前活动，被认为会导致从慢波睡眠过渡到快速眼动睡眠。拟议的研究将调查大鼠快速眼动睡眠发育减少期间（发生在出生后 10 至 30 天之间）胆碱能输入到 SubC 的发展，以及 PPN 驱动 SubC 细胞的能力。我们假设 P 波可能是由间隙连接促进的，我们将研究这种机制作为该系统病理学基础的潜力。