期刊
JOURNAL OF NEUROPHYSIOLOGY
卷 108, 期 1, 页码 148-159出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00839.2011
关键词
motor; mutant; sensory; spinal cord
资金
- National Science and Engineering Research Council of Canada
- Canadian Institutes of Health Research
- Groupe de Recherche sur le Systeme Nerveux Central from Fond de Recherche en Sante du Quebec
- American Cancer Society
- National Institutes of Health
- McKnight Endowment Fund for Neuroscience
Low SE, Woods IG, Lachance M, Ryan J, Schier AF, Saint-Amant L. Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b. J Neurophysiol 108: 148-159, 2012. First published April 4, 2012; doi:10.1152/jn.00839.2011.-The molecular and physiological basis of the touch-unresponsive zebrafish mutant fakir has remained elusive. Here we report that the fakir phenotype is caused by a missense mutation in the gene encoding voltage-gated calcium channel 2.1b (CACNA1Ab). Injection of RNA encoding wild-type CaV2.1 restores touch responsiveness in fakir mutants, whereas knockdown of CACNA1Ab via morpholino oligonucleotides recapitulates the fakir mutant phenotype. Fakir mutants display normal current-evoked synaptic communication at the neuromuscular junction but have attenuated touch-evoked activation of motor neurons. NMDA-evoked fictive swimming is not affected by the loss of CaV2.1b, suggesting that this channel is not required for motor pattern generation. These results, coupled with the expression of CACNA1Ab by sensory neurons, suggest that CaV2.1b channel activity is necessary for touch-evoked activation of the locomotor network in zebrafish.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据