期刊
JOURNAL OF NEUROSCIENCE
卷 29, 期 32, 页码 10063-10071出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1312-09.2009
关键词
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资金
- Association Francaise contre les Myopathies
- Ministere de la Recherche
- French Minister for Foreign Affairs
- National Institutes of Health [R01 EY13160]
- Macular Vision Research Foundation
We investigated the molecular determinants of Ca2+-activated chloride current (CaCC) expressed in adult sensory neurons after a nerve injury. Dorsal root ganglia express the transcripts of three gene families known to induce CaCCs in heterologous systems: bestrophin, tweety, and TMEM16. We found with quantitative transcriptional analysis and in situ hybridization that nerve injury induced upregulation of solely bestrophin-1 transcripts in sensory neurons. Gene screening with RNA interference in single neurons demonstrated that mouse Best1 is required for the expression of CaCC in injured sensory neurons. Transfecting injured sensory neurons with bestrophin-1 mutants inhibited endogenous CaCC. Exogenous expression of the fusion protein green fluorescent protein-Bestrophin-1 in naive neurons demonstrated a plasma membrane localization of the protein that generates a CaCC with biophysical and pharmacological properties similar to endogenous CaCC. Our data suggest that Best1 belongs to a group of genes upregulated by nerve injury and supports functional CaCC expression in injured sensory neurons.
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