東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Behavioral and Biochemical Consequen...

Atrooz, Fatin.

FindBook

Google Book

Amazon

博客來

Behavioral and Biochemical Consequences of Early Life Sleep Deprivation in Rats.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Behavioral and Biochemical Consequences of Early Life Sleep Deprivation in Rats./
作者:	Atrooz, Fatin.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
面頁冊數:	184 p.
附註:	Source: Dissertations Abstracts International, Volume: 80-10, Section: B.
Contained By:	Dissertations Abstracts International80-10B.
標題:	Behavioral psychology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=13837292
ISBN:	9780438845190

Behavioral and Biochemical Consequences of Early Life Sleep Deprivation in Rats.
Atrooz, Fatin.

Behavioral and Biochemical Consequences of Early Life Sleep Deprivation in Rats. - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 184 p.

Source: Dissertations Abstracts International, Volume: 80-10, Section: B.

Thesis (Ph.D.)--University of Houston, 2018.

This item must not be sold to any third party vendors.

Adequate sleep is essential for normal brain function, especially during the critical period of early developmental stages (childhood and adolescence). Many epidemiological and clinical studies have linked early life sleep deprivation (SD) with the occurrence of later life behavioral impairment. However, the mechanism by which early life SD causes behavioral impairment is not fully understood. Animal studies have provided useful insights. Previous reports from our laboratory have suggested a potential role for oxidative stress in induction of behavioral impairments in a rat model of acute sleep deprivation. Others have reported that extended wakefulness increases cellular metabolism and induces formation of reactive oxygen species leading to oxidative stress. Moreover, synaptic pruning and neuronal myelination occurs during early life. These processes are essential for neural circuitry maturation which underlies the behavioral changes. Sleep enhances synaptic pruning and neuronal myelination, strengthening neuronal connections. Therefore, we suggested that sleep deprivation during early life, by engaging stress pathway(s), adversely affects neuronal development and function leading to long-lasting behavioral impairment. We examined the effect of early life SD in rats. The rats at postnatal day (PND) 19 were exposed to SD 6-8h/day for 14 days. The behavioral consequences of SD were examined at different developmental stages; early adolescent: PND33, late adolescent: PND60, and adulthood: PND90. The biochemical markers of stress and synaptic density/ plasticity were measured in different brain regions at PND33 and PND90. We found that anxiety-like behavior was induced in SD rats at early life (PND33 and 60). However, at later life (PND90), anxiety-like behavior disappeared and depression-like behavior developed. Interestingly, we found a reduction in synaptic density and plasticity in prefrontal cortex (PFC) of SD rats at PND33 and PND90 as compared to control rats. The protein level of the stress response phosphatase (MKP1), was upregulated while the protein level of the neurotrophic factor (BDNF) was down-regulated in PFC of SD rats. The results suggest that PND 19-32 in rats (2-11 years in humans), is a sensitive period to SD. Sleep deprivation during this developmental stage alters cortical maturation most likely by reducing synaptic density and plasticity contributing to the behavioral deficits.

ISBN: 9780438845190Subjects--Topical Terms:

2122788
Behavioral psychology.

Behavioral and Biochemical Consequences of Early Life Sleep Deprivation in Rats.
LDR:03618nmm a2200349 4500 001 2209558
005 20191105130509.5
008 201008s2018 ||||||||||||||||| ||eng d
020 $a 9780438845190
035 $a (MiAaPQ)AAI13837292
035 $a (MiAaPQ)0087vireo:4302Atrooz
035 $a AAI13837292
040 $a MiAaPQ $c MiAaPQ
100 1 $a Atrooz, Fatin. $3 3436648
245 1 0 $a Behavioral and Biochemical Consequences of Early Life Sleep Deprivation in Rats.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2018
300 $a 184 p.
500 $a Source: Dissertations Abstracts International, Volume: 80-10, Section: B.
500 $a Publisher info.: Dissertation/Thesis.
500 $a Advisor: Salim, Samina.
502 $a Thesis (Ph.D.)--University of Houston, 2018.
506 $a This item must not be sold to any third party vendors.
506 $a This item must not be added to any third party search indexes.
520 $a Adequate sleep is essential for normal brain function, especially during the critical period of early developmental stages (childhood and adolescence). Many epidemiological and clinical studies have linked early life sleep deprivation (SD) with the occurrence of later life behavioral impairment. However, the mechanism by which early life SD causes behavioral impairment is not fully understood. Animal studies have provided useful insights. Previous reports from our laboratory have suggested a potential role for oxidative stress in induction of behavioral impairments in a rat model of acute sleep deprivation. Others have reported that extended wakefulness increases cellular metabolism and induces formation of reactive oxygen species leading to oxidative stress. Moreover, synaptic pruning and neuronal myelination occurs during early life. These processes are essential for neural circuitry maturation which underlies the behavioral changes. Sleep enhances synaptic pruning and neuronal myelination, strengthening neuronal connections. Therefore, we suggested that sleep deprivation during early life, by engaging stress pathway(s), adversely affects neuronal development and function leading to long-lasting behavioral impairment. We examined the effect of early life SD in rats. The rats at postnatal day (PND) 19 were exposed to SD 6-8h/day for 14 days. The behavioral consequences of SD were examined at different developmental stages; early adolescent: PND33, late adolescent: PND60, and adulthood: PND90. The biochemical markers of stress and synaptic density/ plasticity were measured in different brain regions at PND33 and PND90. We found that anxiety-like behavior was induced in SD rats at early life (PND33 and 60). However, at later life (PND90), anxiety-like behavior disappeared and depression-like behavior developed. Interestingly, we found a reduction in synaptic density and plasticity in prefrontal cortex (PFC) of SD rats at PND33 and PND90 as compared to control rats. The protein level of the stress response phosphatase (MKP1), was upregulated while the protein level of the neurotrophic factor (BDNF) was down-regulated in PFC of SD rats. The results suggest that PND 19-32 in rats (2-11 years in humans), is a sensitive period to SD. Sleep deprivation during this developmental stage alters cortical maturation most likely by reducing synaptic density and plasticity contributing to the behavioral deficits.
590 $a School code: 0087.
650 4 $a Behavioral psychology. $3 2122788
650 4 $a Developmental psychology. $3 516948
650 4 $a Experimental psychology. $3 2144733
690 $a 0384
690 $a 0620
690 $a 0623
710 2 $a University of Houston. $b Pharmacological and Pharmaceutical Sciences. $3 3436649
773 0 $t Dissertations Abstracts International $g 80-10B.
790 $a 0087
791 $a Ph.D.
792 $a 2018
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=13837292