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Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b

Low, Sean E. and Woods, Ian G. and Lachance, Mathieu and Ryan, Joel and Schier, Alexander F. and Saint-Amant, Louis. (2012) Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b. Journal of Neurophysiology, 108 (1). pp. 148-159.

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Official URL: https://edoc.unibas.ch/74709/

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Abstract

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.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Growth & Development > Cell and Developmental Biology (Schier)
UniBasel Contributors:Schier, Alexander F
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:American Physiological Society
ISSN:0022-3077
e-ISSN:1522-1598
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:16 Dec 2020 17:17
Deposited On:16 Dec 2020 17:17

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