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Gene expression and plasticity in the rat auditory cortex after bilateral cochlear ablation
Cited 15 time in
Web of Science
Cited 16 time in Scopus
- Authors
- Issue Date
- 2007
- Publisher
- Taylor & Francis
- Citation
- Acta Otolaryngol 2007;127:341-50
- Keywords
- Central auditory system ; damage protection ; genes ; auditory cortex ; critical period ; microarray analysis ; deafness
- Abstract
- CONCLUSION: The plastic changes in the auditory cortex after bilateral cochlear ablation are related to the immediate early genes as well as the neural plasticity-related genes. In addition, cross-modal plasticity may play an important role in the early changes in the auditory cortex after bilateral cochlear ablation. OBJECTIVES: The purpose of this study was to identify candidate genes involved in the normal development of primary auditory cortex during the critical period as well as those genes specifically modulated under conditions of sensory deafferentation by bilateral cochlear ablation. MATERIALS AND METHODS: We produced a bilaterally deaf rat model and used DNA microarray technology to analyze differential gene expression in the primary auditory cortex of bilateral cochlear ablated and sham-operated age-matched control rats. Gene expression in the auditory cortex was compared at 2, 4, and 12 weeks after surgery. For selected genes, the changes in gene expression were confirmed by real-time polymerase chain reaction (PCR). RESULTS: In the cochlear ablation groups, the expression of immediate early genes (Egr1, 2, 3, 4, c-fos, etc.) and neural plasticity-related genes (Arc, Syngr1, Bdnf, etc.) was decreased at 2 weeks and increased at 4 weeks. The expression of neurotransmission-related genes (Gabra5, Chrnb3, Chrne, etc.) was decreased at 12 weeks.
- ISSN
- 0001-6489 (Print)
- Language
- English
- URI
- http://www.informaworld.com/smpp/content~db=all?content=10.1080/00016480701275246
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17453451
https://hdl.handle.net/10371/11168
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