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Impact of early life sleep deprivation on later life behaviors in rats
Author(s) -
Atrooz Fatin,
Liu Hesong,
Kochi Camila,
Salim Samina
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.554.12
Subject(s) - sleep deprivation , privation , anxiety , sleep (system call) , maternal deprivation , corticosterone , depression (economics) , psychology , elevated plus maze , medicine , oxidative stress , cognition , endocrinology , physiology , psychiatry , computer science , hormone , operating system , economics , macroeconomics
Increasing body of epidemiological studies suggest that sleep deprivation at early life stages (childhood and adolescence) is associated with behavioral and cognitive impairment. While these studies are important, yet, the relationship between early life sleep deprivation and development of later life psychiatric symptoms is not clearly understood. While examining the link between early life sleep deprivation and later life behavioral and cognitive well‐being is important, conducting such clinical studies in children are difficult. Therefore, animal models are valuable in studying the behavioral and biochemical consequences of early life sleep deprivation across the developmental course. Extended wakefulness increases cellular metabolism and induces reactive oxygen species (ROS) formation leading to oxidative stress. Hence, we examined the role of oxidative stress on behavioral impairment caused by early life SD. We employed two groups of male Sprague Dawley rats; control (CON) and sleep deprivation (SD) groups. Rats, at postnatal day (PND) 19 were subjected to SD for 14 days, (6–8 hours/day) using Pinnacle automated sleep deprivation system. Behavioral and cognitive tests were performed at three stages; early adolescent (PND32), late adolescent (PND60) and adult stage (PND90). Rats in the SD group exhibited anxiety‐like behavior at PND32 and 60 but not at PND90. Interestingly, SD rats did not exhibit depression‐like behavior at PND32 or at PND60 but developed depression‐like behavior at PND90, as indicated by increased immobility time in forced swim test compared to control group. Plasma levels of corticosterone (indicator of stress) were significantly increased in SD rats compared to control rats. We conclude that early life sleep deprivation during postnatal brain development, by engaging oxidative stress cascades, might alter the normal synapse formation and pruning causing anxiety‐like behavior early in life (at PND32 and 60), which in later life transforms into depression‐like behavior (PND 90). Support or Funding Information 2R15MH093918‐02 This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .