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