The effect of P2X7 receptor activation on nuclear factor-κB phosphorylation induced by status epilepticus in the rat hippocampus.

Nuclear factor-kappa B (NFκB) signal is essential for neuronal survival and its activation may protect neuron against various stimuli. Since purinergic signals activate NFκB through the P2X7 receptor, we investigated the distinct pattern of NF-κB phosphorylation in neurons by P2X7 receptor activation following status epilepticus (SE) in an effort to understand the role of P2X7 receptor in epileptogenic insult. In non-SE animals, 2'(3')-O-(4-benzoyl)benzoyl adenosine 5'-triphosphate (BzATP, a P2X7R agonist) treatment increased only p52-Ser869 NF-κB phosphorylation in neuron. Following SE, p52-Ser865, p52-Ser869, p65-Ser276, p65-Ser311, p65-Ser468, and p65-Ser529 NF-κB phosphorylation was significantly decreased in CA1 and CA3 neurons. However, BzATP treatment prevented reductions in p65-Ser276, p65-Ser311, p65-Ser529, and p52-Ser869 NF-κB phosphorylations in CA1 and/or CA3 neurons induced by SE. Furthermore, BzATP treatment reduced SE-induced p65-Ser311, p65-Ser468, p65-Ser536, and p52-Ser869 NF-κB phosphorylations in astrocytes. These findings indicate that P2X7 functions may be involved in the regulation of SE-induced reactive astrocytes and neuronal degeneration via NF-κB phosphorylations in response to pilocarpine-induced SE in the rat hippocampus.