title: Differential nuclear factor-kappa B phosphorylation induced by lipopolysaccharide in the hippocampus of P2X7 receptor knockout mouse.
abstract: OBJECTIVE
  Lipopolysaccharide (LPS) stimulates the innate immune response in the brain through nuclear factor-kappaB (NF-kappaB) signaling. Since purinergic signals activate NF-kappaB through the P2X7 receptor (P2X7R), we investigated the roles of P2X7R in neuronal NF-kappaB phosphorylation in the mouse hippocampus under basal conditions and P2X7R deletion following LPS treatment in vivo.
  
  
  METHODS
  We performed immunohistochemical studies for neuronal NF-kappaB phosphorylation in the hippocampi of wild type (WT) and P2X7R knockout (KO) mice under basal conditions and LPS treatment.
  
  
  RESULTS
  LPS treatment did not induce neuronal damages in both WT and P2X7(-/-) KO mice. In WT animals, LPS treatment increased p65-Ser276 and p65-Ser311 NF-kappaB phosphorylations in hippocampal neurons. However, p52-Ser865, p52-Ser869, p65-Ser468, p65-Ser529, and p65-Ser536 NF-kappaB phosphorylations were unaffected by LPS treatment. In P2X7(-/-) KO mice, neuronal p65-Ser311 NF-kappaB phosphorylation in vehicle-treated animals was higher than that in WT animals. In addition, both p65-Ser276 and p65-Ser311 NF-kappaB phosphorylations were unaffected by LPS treatment in P2X7(-/-) KO mice.
  
  
  CONCLUSIONS
  These findings indicate that P2X7R may be involved in LPS-induced inflammatory response in neurons, and that p65-Ser311 NF-kappaB phosphorylation may compensate for the loss function of P2X7R by as yet unknown factors.
authors.affiliation: Department of Anatomy and Neurobiology, Institute of Epilepsy Research, College of Medicine, Hallym University, Kangwon-Do, Korea.
authors.forename: Won Il
authors.initials: WI
authors.lastname: Kim
authors.forename: Hea Jin
authors.initials: HJ
authors.lastname: Ryu
authors.forename: Ji-Eun
authors.initials: JE
authors.lastname: Kim
authors.forename: Cheong Hoon
authors.initials: CH
authors.lastname: Seo
authors.forename: Boung Chul
authors.initials: BC
authors.lastname: Lee
authors.forename: Ihn-Geun
authors.initials: IG
authors.lastname: Choi
authors.forename: Tae-Cheon
authors.initials: TC
authors.lastname: Kang
mesh_terms: D000818:Animals; D006624:Hippocampus / Q000378:metabolism*; D007150:Immunohistochemistry; D007249:Inflammation / Q000235:genetics / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016328:NF-kappa B / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D010766:Phosphorylation; D058486:Receptors, Purinergic P2X7 / Q000172:deficiency* / Q000235:genetics; D015398:Signal Transduction / Q000502:physiology*; D051996:Transcription Factor RelA / Q000378:metabolism*
chemical_list: D008070:Lipopolysaccharides; D016328:NF-kappa B; D058486:Receptors, Purinergic P2X7; C498144:Rela protein, mouse; D051996:Transcription Factor RelA