PMID- 26622210
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20151201
LR  - 20200929
IS  - 1611-2156 (Print)
IS  - 1611-2156 (Electronic)
IS  - 1611-2156 (Linking)
VI  - 12
DP  - 2013
TI  - .
PG  - 347-72
AB  - Experimentally-induced total sleep deprivation (TSD) and chronic partial sleep 
      restriction (CPSR) leads to the emergence of cognitive impairments. This is 
      hypothesized to result from a consequent neuroinflammation which may also hasten 
      the neurodegenerative processes. Neuroinflammatory markers such as tumor necrosis 
      factor-alpha (TNFalpha) are thought to be potential culprits in SD-induced 
      neurodegeneration. The effect of TSD and CPSR on memory and anxiety-related 
      behaviors (using the Elevated Plus-Maze test-retest protocol) and serum level of 
      brain derived neurotrophic factor (BDNF) and corticosterone were assessed in male 
      Wistar rats subjected to the modified disk-over-water (DOW) apparatus. In 
      addition, an immunohistochemical (IHC) study was done to possibly detect the 
      amyloid-beta (Abeta) and hyper-phosphorylated tau protein (HPtau) deposition in the 
      dentate gyrus (DG) of the examined rats' hippocampi. Histomorphology and neuronal 
      numerical density assessments were done at the same level across control and 
      experimental animals. We also studied the above parameters in rats after 
      intraperitoneal injection of the TNFalpha neutralizing antibody, infliximab (IFX). 
      Rats subjected to TSD and CPSR which did not receive IFX, showed a more 
      pronounced impairment of memory, elevated serum corticosterone and decreased BDNF 
      levels. CPSR rats which underwent delayed brain excision following behavioral 
      testing, showed deposition of the HPtau and revealed the least numerical density in 
      the hippocampal DG neurons. Meanwhile, IHC study revealed no Abeta deposition in the 
      hippocampal DG of all examined rats. Interestingly, treatment with IFX, abrogated 
      sleep restriction-induced cognitive decline, biochemical changes and the 
      immunohistopathology in the hippocampal DG. Taken together, our findings 
      indicated that CPSR (the SD model mimicking shift work) induces not only 
      cognitive and biochemical changes, but also pathology in the hippocampal DG. This 
      is possibly via activation of the inflammatory mechanisms in part through 
      TNFalpha-dependent pathways.
FAU - Torabi-Nami, Mohammad
AU  - Torabi-Nami M
AD  - Institute for Cognitive Science Studies, Tehran, Iran ; Department of 
      Neuroscience, School of Advanced Medical Science and Technologies, Shiraz 
      University of Medical Sciences, Shiraz, Iran.
FAU - Nasehi, Mohammad
AU  - Nasehi M
AD  - Department of Biology, Faculty of Basic Sciences, Islamic Azad University, 
      Garmsar branch, Garmsar, Iran.
FAU - Zarrindast, Mohammad-Reza
AU  - Zarrindast MR
AD  - Institute for Cognitive Science Studies, Tehran, Iran ; Department Neuroscience, 
      Advanced School of Medical Technologies and Department of Pharmacology, School of 
      Medicine, Tehran University of Medical Sciences, Tehran, Iran ; Iranian National 
      Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran 
      ; Institute for Studies in Theoretical Physics and Mathematics, School of 
      Cognitive Sciences, Tehran, Iran.
LA  - eng
PT  - Journal Article
DEP - 20130414
PL  - Germany
TA  - EXCLI J
JT  - EXCLI journal
JID - 101299402
PMC - PMC4663654
OTO - NOTNLM
OT  - BDNF
OT  - corticosterone
OT  - dentate gyrus
OT  - elevated plus-maze
OT  - immunohistochemistry
OT  - infliximab
OT  - rat(s)
OT  - sleep deprivation
EDAT- 2013/01/01 00:00
MHDA- 2013/01/01 00:01
PMCR- 2013/04/14
CRDT- 2015/12/02 06:00
PHST- 2013/03/21 00:00 [received]
PHST- 2013/04/30 00:00 [accepted]
PHST- 2015/12/02 06:00 [entrez]
PHST- 2013/01/01 00:00 [pubmed]
PHST- 2013/01/01 00:01 [medline]
PHST- 2013/04/14 00:00 [pmc-release]
AID - 2013-209 [pii]
AID - Doc347 [pii]
PST - epublish
SO  - EXCLI J. 2013 Apr 14;12:347-72. eCollection 2013.