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Upregulation of NF-kappaB p50 during neuronal adaptation after chemotoxic injury to the hippocampus.
Kassed-CA; Phelps-CP; O'Callaghan-JP; Pennypacker-KR
Abstr - Soc Neurosci 2000 Nov; 26:1
NF-kB p50 transcription factor levels throughout the rodent hippocampus are upregulated in surviving neurons twenty-four hours after a single injection of trimethyltin (TMT), the well-characterized neurotoxicant with exquisite selectivity toward stannin-expressing neurons. p50-expressing neurons are not positive for Fluoro-Jade, a marker of neuronal degeneration, at seven days after chemotoxic insult, and the pattern of degeneration differs from that observed after transient ischemic injury. Nerve growth factor (NGF), a neurotrophin whose gene is a target of NF-kB, follows a time course of increased expression paralleling that of p50, suggesting involvement of this NF-kB- regulated gene in neural repair processes. Co-localization studies of p50, NGF, and stannin-containing cells allows detailed characterization of the subset of neurons responding to injury. Immunohistochemical staining of NGF-positive hippocampal tissue for p50 expression enables localization of both proteins, while determination of neuronal survivability after TMT treatment of p50-/- transgenic mice establishes the specific functional relationship of p50 to neuronal survival in the intact murine hippocampus. Upregulation of p50 in the brain injury response is implicated in the activation of genes related to regeneration and repair.
Pharmacology; Growth-factors; Neurotoxins; Neurotoxic-effects; Neurotoxicity; Animal-studies; Laboratory-animals; Central-nervous-system; Central-nervous-system-disorders
Abstract; Conference/Symposia Proceedings
Abstracts - Society for Neuroscience. Society for Neuroscience's 30th Annual Meeting, New Orleans, LA, November 4 - 9, 2000