Related Experiment Video
Updated: May 12, 2026
Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis
Published on: February 13, 2014
Differential nuclear factor-kappa B phosphorylation induced by lipopolysaccharide in the hippocampus of P2X7 receptor
Won Il Kim1, Hea Jin Ryu, Ji-Eun Kim
1Department of Anatomy and Neurobiology, Institute of Epilepsy Research, College of Medicine, Hallym University, Kangwon-Do, Korea.
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.
Discussion:
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.
