ArticleJournal of neurophysiology2012
Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b.
Article in Journal of neurophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed.
- Review
- Review
- Genetic modeling of degenerative diseases and mechanisms of neuronal regeneration in the zebrafish cerebellum.Cellular and molecular life sciences : CMLS · 2024Review
- Localization of Piezo 1 and Piezo 2 in Lateral Line System and Inner Ear of Zebrafish (International journal of molecular sciences · 2024Article
- Zebrafish Models of Rare Neurological Diseases like Spinocerebellar Ataxias (SCAs): Advantages and Limitations.Biology · 2023Review
- Towards Zebrafish Models of CNS Channelopathies.International journal of molecular sciences · 2022Review
- A forward genetic screen identifies Dolk as a regulator of startle magnitude through the potassium channel subunit Kv1.1.PLoS genetics · 2021Article
- Zebrafish Models of Autosomal Dominant Ataxias.Cells · 2021Review
- Review
- Phenotypic Characterization of Larval Zebrafish (Danio rerio) with Partial Knockdown of the cacna1a Gene.Molecular neurobiology · 2020Article
- Zebrafish as a Model System for the Study of Severe CaFrontiers in molecular neuroscience · 2019Review
- Zebrafish: an emerging real-time model system to study Alzheimer's disease and neurospecific drug discovery.Cell death discovery · 2018Article
- Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016Review
- pigk Mutation underlies macho behavior and affects Rohon-Beard cell excitability.Journal of neurophysiology · 2015Article
- RING finger protein 121 facilitates the degradation and membrane localization of voltage-gated sodium channels.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Discovering novel neuroactive drugs through high-throughput behavior-based chemical screening in the zebrafish.Frontiers in pharmacology · 2014Review
- Zebrafish calls for reinterpretation for the roles of P/Q calcium channels in neuromuscular transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Validation of the zebrafish pentylenetetrazol seizure model: locomotor versus electrographic responses to antiepileptic drugs.PloS one · 2013Article
- Developing a pathway to clinical trials forTherapeutic advances in rare diseaseReview
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Authors and funding
6 authors.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.