TNFR2 mediated TNF-α signaling and Nf-κB activation in hippocampus of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice

Publication date: Available online 23 February 2018
Source:Neuroscience Research
Author(s): Nabanita Ghosh, Soham Mitra, Priyobrata Sinha, Nilkanta Chakrabarti, Arindam Bhattacharyya
1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP) −induced neuroinflammation and its impact in hippocampus remain elusive till date. Our present study includes the time dependent changes of inflammatory molecules in mouse hippocampus during MPTP treatment. MPTP treatment increased level of TNF-α, enhanced expression of TNFR2 along with PI3 kinase (PI3K) induced phosphorylation of Akt resulting in persistent nuclear factor-κB (NF-κB) activation. The expressions gradually increased from Day1 post-MPTP treatment, maximally at Day3 post-treatment. MPTP induced translocation of p65 and p52, two subunits of NF-κB family, to nucleus where they had been found to dimerize. Therefore, MPTP induced TNF-α signaling through TNFR2 mediated pathway and recruited p65-p52 dimer in hippocampal nucleus which is reported to have protective effect on hippocampal neurons indicated by unchanged neuronal count in hippocampus in treated groups with respect to control. Our finding suggests that this unique NF-κB dimer plays some role in providing inherent protection to hippocampus during MPTP-treatment.



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