Journal
JOURNAL OF COMPARATIVE NEUROLOGY
Volume 521, Issue 5, Pages 1165-1183Publisher
WILEY
DOI: 10.1002/cne.23227
Keywords
apoptosis; cell death; protein synthesis; cochlea removal; afferent deprivation; nucleus magnocellularis
Categories
Funding
- National Institute on Deafness and Other Communication Disorders [DC-03829, DC-02739, DC-04661, DC-00018]
- Deafness Research Foundation
- University of Washington Mary Gates Endowment
Ask authors/readers for more resources
The relationships between protein synthesis and neuronal survival are poorly understood. In chicken nucleus magnocellularis (NM), significant alterations in overall protein synthesis precede neuronal death induced by deprivation of excitatory afferent activity. Previously we demonstrated an initial reduction in the overall rate of protein synthesis in all deprived NM neurons, followed by quick recovery (starting at 6 hours) in some, but not all, neurons. Neurons with recovered protein synthesis ultimately survive, whereas others become ghost cells (no detectable Nissl substance) at 1224 hours and die within 48 hours. To explore the mechanisms underlying this differential influence of afferent input on protein synthesis and cell survival, the current study investigates the involvement of eukaryotic translation elongation factor 2 (eEF2), the phosphorylation of which reduces overall protein synthesis. Using immunocytochemistry for either total or phosphorylated eEF2 (p-eEF2), we found significant reductions in the level of phosphorylated, but not total, eEF2 in NM neurons as early as 0.51 hour following cochlea removal. Unexpectedly, neurons with low levels of p-eEF2 show reduced protein synthesis at 6 hours, indicated by a marker for active ribosomes. At 12 hours, all ghost cells exhibited little or no p-eEF2 staining, although not every neuron with a comparable low level of p-eEF2 was a ghost cell. These observations demonstrate that a reduced level of p-eEF2 is not responsible for immediate responses (including reduced overall protein synthesis) of a neuron to compromised afferent input but may impair the neuron's ability to initiate recovery signaling for survival and make the neuron more vulnerable to death. J. Comp. Neurol. 521:11651183, 2013. (c) 2012 Wiley Periodicals, Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available