Abstract:
:The roles of activated NF-kappaB subunits in the CNS remain to be discerned. Members of this family of transcription factors are essential to diverse physiological processes and can be activated by pathogens, stress, pharmacological agents, and trauma. We are particularly interested in long-term NF-kappaB activation and its involvement in neuroplastic changes in the brain resulting from acquisition of memory as well as injury. Here, we use lesioning by the limbic-specific neurotoxicant trimethyltin (TMT) as a model in which to examine activation of the NF-kappaB p50 subunit before, during, and after neuronal degeneration. Neurons in wild-type mice that survived TMT-induced injury contained activated p50 and did not label with Fluoro-Jade, a histochemical marker of degenerating neurons. Granule cells of the wild-type dentate gyrus subregion, an area particularly vulnerable to TMT-induced degeneration, contained less activated p50 protein than CA regions. We compared the extent of degeneration in wild-type and p50-null mice and found a fivefold increase in death of hippocampal neurons in mice lacking p50. The hippocampus is key to processes of learning and memory, and NF-kappaB has reported involvement in these processes. The enhanced hippocampal degeneration in p50-null mice prompted us to evaluate their basal learning abilities, and we discovered that difficulties in task acquisition were an additional consequence of p50 ablation. These results indicate that absence of p50 negatively modulates learning ability as well as hippocampal responsiveness to brain injury after a chemical-induced lesion.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Kassed CA,Willing AE,Garbuzova-Davis S,Sanberg PR,Pennypacker KRdoi
10.1006/exnr.2002.7967keywords:
subject
Has Abstractpub_date
2002-08-01 00:00:00pages
277-88issue
2eissn
0014-4886issn
1090-2430pii
S0014488602979677journal_volume
176pub_type
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journal_title:Experimental neurology
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journal_title:Experimental neurology
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