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
-
- Valine/genetics
- Mutagenesis, Site-Directed/methods
- Nicotinic Antagonists/pharmacology
- Nerve Net/physiology
- Afferent Pathways/physiology
- Dose-Response Relationship, Drug
- Humans
- Calcium Channels, N-Type/genetics
- Calcium Channels, N-Type/metabolism*
- Spinal Cord/cytology
- Spinal Cord/physiology
- Mutation/genetics
- Escape Reaction/drug effects
- Escape Reaction/physiology
- Locomotion/drug effects
- Locomotion/genetics
- Curare/pharmacology
- Motor Activity/genetics
- Synaptic Transmission/drug effects
- Synaptic Transmission/genetics
- HEK293 Cells
- Acetylcholine/pharmacology
- Morpholines/pharmacology
- Embryo, Nonmammalian
- Zebrafish
- Evoked Potentials/genetics
- Animals
- Motor Neurons/drug effects
- Ion Channel Gating/drug effects
- Ion Channel Gating/genetics*
- Mutation, Missense/genetics
- Bungarotoxins/metabolism
- Touch/genetics*
- Touch/physiology
- Muscle, Skeletal/drug effects
- Muscle, Skeletal/physiology
- Leucine/genetics
- Animals, Genetically Modified
- Action Potentials/drug effects
- Action Potentials/genetics
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- Models, Molecular
- PubMed
- 22490555 Full text @ J. Neurophysiol.
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.