PUBLICATION

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

Authors
Low, S.E., Woods, I.G., Lachance, M., Ryan, J., Schier, A.F., and Saint-Amant, L.
ID
ZDB-PUB-120412-3
Date
2012
Source
Journal of neurophysiology   108(1): 148-159 (Journal)
Registered Authors
Low, Sean, Saint-Amant, Louis, Schier, Alexander, Woods, Ian G.
Keywords
spinal cord, mutant, zebrafish, sensory, motor
MeSH Terms
  • Leucine/genetics
  • Nerve Net/physiology
  • Synaptic Transmission/drug effects
  • Synaptic Transmission/genetics
  • Ion Channel Gating/drug effects
  • Ion Channel Gating/genetics*
  • Afferent Pathways/physiology
  • Humans
  • Mutation, Missense/genetics
  • HEK293 Cells
  • Evoked Potentials/genetics
  • Calcium Channels, N-Type/genetics
  • Calcium Channels, N-Type/metabolism*
  • Escape Reaction/drug effects
  • Escape Reaction/physiology
  • Models, Molecular
  • Bungarotoxins/metabolism
  • Nicotinic Antagonists/pharmacology
  • Locomotion/drug effects
  • Locomotion/genetics
  • Motor Neurons/drug effects
  • Zebrafish
  • Mutagenesis, Site-Directed/methods
  • Touch/genetics*
  • Touch/physiology
  • Animals
  • Dose-Response Relationship, Drug
  • Action Potentials/drug effects
  • Action Potentials/genetics
  • Acetylcholine/pharmacology
  • Mutation/genetics
  • Motor Activity/genetics
  • Embryo, Nonmammalian
  • Morpholines/pharmacology
  • Muscle, Skeletal/drug effects
  • Muscle, Skeletal/physiology
  • Curare/pharmacology
  • Valine/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Animals, Genetically Modified
  • Spinal Cord/cytology
  • Spinal Cord/physiology
(all 43)
PubMed
22490555 Full text @ J. Neurophysiol.
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.

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