PMID- 18687977
OWN - NLM
STAT- MEDLINE
DCOM- 20081106
LR  - 20220227
IS  - 8750-7587 (Print)
IS  - 1522-1601 (Electronic)
IS  - 0161-7567 (Linking)
VI  - 105
IP  - 4
DP  - 2008 Oct
TI  - Spontaneous and influenza virus-induced sleep are altered in TNF-alpha 
      double-receptor deficient mice.
PG  - 1187-98
LID - 10.1152/japplphysiol.90388.2008 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) is associated with sleep regulation in 
      health and disease. Previous studies assessed sleep in mice genetically deficient 
      in the TNF-alpha 55-kDa receptor. In this study, spontaneous and influenza 
      virus-induced sleep profiles were assessed in mice deficient in both the 55-kDa 
      and 75-kDa TNF-alpha receptors [TNF-2R knockouts (KO)] and wild-type (WT) strain 
      controls. Under baseline conditions the TNF-2R KO mice had less non-rapid eye 
      movement sleep (NREMS) than WTs during the nighttime and more rapid eye movement 
      sleep (REMS) than controls during the daytime. The differences between nighttime 
      maximum and daytime minimum values of electroencephalogram (EEG) delta power 
      during NREMS were greater in the TNF-2R KO mice than in WTs. Viral challenge 
      (mouse-adapted influenza X-31) enhanced NREMS and decreased REMS in both strains 
      roughly to the same extent. EEG delta power responses to viral challenge differed 
      substantially between strains; the WT animals increased, whereas the TNF-2R KO 
      mice decreased their EEG delta wave power during NREMS. There were no differences 
      between strains in body temperatures or locomotor activity in uninfected mice or 
      after viral challenge. Analyses of cortical mRNAs confirmed that the TNF-2R KO 
      mice lacked both TNF-alpha receptors; these mice also had higher levels of orexin 
      mRNA and reduced levels of the purine P2X7 receptor compared with WTs. Results 
      reinforce the hypothesis that TNF-alpha is involved in physiological sleep 
      regulation but plays a limited role in the acute-phase response induced by 
      influenza virus.
FAU - Kapas, Levente
AU  - Kapas L
AD  - Department of Biological Sciences, Fordham University, Bronx, NY 10458, USA. 
      kapas@fordham.edu
FAU - Bohnet, Stewart G
AU  - Bohnet SG
FAU - Traynor, Tim R
AU  - Traynor TR
FAU - Majde, Jeannine A
AU  - Majde JA
FAU - Szentirmai, Eva
AU  - Szentirmai E
FAU - Magrath, Paul
AU  - Magrath P
FAU - Taishi, Ping
AU  - Taishi P
FAU - Krueger, James M
AU  - Krueger JM
LA  - eng
GR  - HD 36520/HD/NICHD NIH HHS/United States
GR  - NS 31453/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20080807
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Neuropeptides)
RN  - 0 (Orexins)
RN  - 0 (P2rx7 protein, mouse)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Purinergic P2)
RN  - 0 (Receptors, Purinergic P2X7)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Tnfrsf1a protein, mouse)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Body Temperature
MH  - Cerebral Cortex/*metabolism/physiopathology/virology
MH  - Disease Models, Animal
MH  - Electroencephalography
MH  - Influenza A Virus, H1N1 Subtype/genetics
MH  - Influenza A Virus, H3N2 Subtype/genetics
MH  - Intracellular Signaling Peptides and Proteins/metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Motor Activity
MH  - Neuropeptides/metabolism
MH  - Orexins
MH  - Orthomyxoviridae Infections/*metabolism/physiopathology/virology
MH  - RNA, Messenger/metabolism
MH  - Receptors, Purinergic P2/metabolism
MH  - Receptors, Purinergic P2X7
MH  - Receptors, Tumor Necrosis Factor, Type I/deficiency/genetics/*metabolism
MH  - Receptors, Tumor Necrosis Factor, Type II/deficiency/genetics/*metabolism
MH  - *Sleep Stages
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*metabolism
PMC - PMC2576045
EDAT- 2008/08/09 09:00
MHDA- 2008/11/07 09:00
PMCR- 2009/10/01
CRDT- 2008/08/09 09:00
PHST- 2008/08/09 09:00 [pubmed]
PHST- 2008/11/07 09:00 [medline]
PHST- 2008/08/09 09:00 [entrez]
PHST- 2009/10/01 00:00 [pmc-release]
AID - 90388.2008 [pii]
AID - JAPPL-90388-2008 [pii]
AID - 10.1152/japplphysiol.90388.2008 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2008 Oct;105(4):1187-98. doi: 
      10.1152/japplphysiol.90388.2008. Epub 2008 Aug 7.