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
  • Evoked Potentials/genetics
  • Motor Neurons/drug effects
  • Nerve Net/physiology
  • Zebrafish
  • Mutation, Missense/genetics
  • Animals
  • Dose-Response Relationship, Drug
  • Action Potentials/drug effects
  • Action Potentials/genetics
  • Mutagenesis, Site-Directed/methods
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
  • Valine/genetics
  • Afferent Pathways/physiology
  • Motor Activity/genetics
  • Synaptic Transmission/drug effects
  • Synaptic Transmission/genetics
  • Spinal Cord/cytology
  • Spinal Cord/physiology
  • Bungarotoxins/metabolism
  • Touch/genetics*
  • Touch/physiology
  • Curare/pharmacology
  • Humans
  • Acetylcholine/pharmacology
  • Ion Channel Gating/drug effects
  • Ion Channel Gating/genetics*
  • Embryo, Nonmammalian
  • HEK293 Cells
  • Leucine/genetics
  • Models, Molecular
  • Calcium Channels, N-Type/genetics
  • Calcium Channels, N-Type/metabolism*
  • Nicotinic Antagonists/pharmacology
  • Muscle, Skeletal/drug effects
  • Muscle, Skeletal/physiology
  • Animals, Genetically Modified
  • Morpholines/pharmacology
  • Escape Reaction/drug effects
  • Escape Reaction/physiology
  • Locomotion/drug effects
  • Locomotion/genetics
  • Mutation/genetics
(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.

Genes / Markers
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Human Disease / Model
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