期刊
BRAIN RESEARCH
卷 1203, 期 -, 页码 18-25出版社
ELSEVIER
DOI: 10.1016/j.brainres.2008.01.076
关键词
auditory system; nucleus magnocellularis; cell death, neuroprotection; Bcl-2
资金
- NIDCD NIH HHS [R01 DC000858, R56 DC000858, R56 DC000858-18, DC00858] Funding Source: Medline
The avian brainstem serves as a useful model to answer the question of how afferent activity influences the viability of target neurons. Approximately 20-30% of neurons in the avian cochlear nucleus, nucleus magnocellularis (NM) die following deafferentation (i.e., deafness produced by cochlea removal). Interestingly, Bcl-2 mRNA (but not protein) is upregulated in 20-30% of NM neurons following deafferentation. We have recently shown that chronic treatments of lithium upregulates the neuroprotective protein Bcl-2 and increases neuronal survival following deafferentation. The pathways leading to the upregulation of Bcl-2 expression following these two manipulations are unknown. The present experiments examine changes in glycogen synthase kinase-3 beta (Gsk-3 beta), and transcription factors nuclear factor kappa B (NF kappa B), beta-catenin, and pCreb following lithium administration and following deafferentation. These molecules are known to be influenced by lithium and to regulate Bcl-2 expression in other model systems. Lithium decreased immunolabeling for Gsk-3 beta and increased expression for all three transcription factors. Deafferentation, however, did not alter Gsk-3 beta or NF kappa B, resulted in lower beta-catenin expression, but did increase pCreb immunore activity. While it is possible that pCreb is a common link in the regulation of Bcl-2 following these two manipulations, the timing and distribution of pCreb labeling suggests that it is not the sole determinant of Bcl-2 upregulation following deafferentation. It is likely that the regulation of Bcl-2 gene expression by lithium and by deafferentation involves different molecular pathways. (c) 2008 Elsevier B.V. All rights reserved.
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