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

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.

Pubmed ID: 22490555 RIS Download

Mesh terms: Acetylcholine | Action Potentials | Afferent Pathways | Animals | Animals, Genetically Modified | Bungarotoxins | Calcium Channels, N-Type | Curare | Dose-Response Relationship, Drug | Embryo, Nonmammalian | Escape Reaction | Evoked Potentials | HEK293 Cells | Humans | Ion Channel Gating | Leucine | Locomotion | Models, Molecular | Morpholines | Motor Activity | Motor Neurons | Muscle, Skeletal | Mutagenesis, Site-Directed | Mutation | Mutation, Missense | Nerve Net | Nicotinic Antagonists | Spinal Cord | Synaptic Transmission | Touch | Valine | Zebrafish | Zebrafish Proteins

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