ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
The zebrafish shocked gene encodes a glycine transporter and is essential for the function of early neural circuits in the CNS.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 81 citations in OpenAlex.
- Case Report: Neonatal lethality caused by novel compound heterozygous missense variants ofFrontiers in pediatrics · 2026Article
- Establishment and characterization of adap1-deficient zebrafish.Development, growth & differentiation · 2025Article
- Impaired glycine neurotransmission causes adolescent idiopathic scoliosis.The Journal of clinical investigation · 2024Article
- Single-Cell RNA Sequencing Characterizes the Molecular Heterogeneity of the Larval Zebrafish Optic Tectum.Frontiers in molecular neuroscience · 2022Article
- Article
- The presynaptic glycine transporter GlyT2 is regulated by the Hedgehog pathway in vitro and in vivo.Communications biology · 2021Article
- Functional and Biochemical Consequences of Disease Variants in Neurotransmitter Transporters: A Special Emphasis on Folding and Trafficking Deficits.Pharmacology & therapeutics · 2021Review
- Elevated preoptic brain activity in zebrafish glial glycine transporter mutants is linked to lethargy-like behaviors and delayed emergence from anesthesia.Scientific reports · 2021Article
- Behavioral and brain- transcriptomic synchronization between the two opponents of a fighting pair of the fish Betta splendens.PLoS genetics · 2020Article
- Single-Cell Reconstruction of Emerging Population Activity in an Entire Developing Circuit.Cell · 2019Article
- Individual knock out of glycine receptor alpha subunits identifies a specific requirement of glra1 for motor function in zebrafish.PloS one · 2019Article
- Structural Neural Connectivity Analysis in Zebrafish With Restricted Anterograde Transneuronal Viral Labeling and Quantitative Brain Mapping.Frontiers in neural circuits · 2019Article
- Glycine decarboxylase deficiency-induced motor dysfunction in zebrafish is rescued by counterbalancing glycine synaptic level.JCI insight · 2018Article
- Investigation of hindbrain activity during active locomotion reveals inhibitory neurons involved in sensorimotor processing.Scientific reports · 2018Article
- Zebrafish: A Pharmacogenetic Model for Anesthesia.Methods in enzymology · 2018Article
- Expansion microscopy of zebrafish for neuroscience and developmental biology studies.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- In Vivo Measurement of Glycine Receptor Turnover and Synaptic Size Reveals Differences between Functional Classes of Motoneurons in Zebrafish.Current biology : CB · 2017Article
- Loss of Glycine Transporter 1 Causes a Subtype of Glycine Encephalopathy with Arthrogryposis and Mildly Elevated Cerebrospinal Fluid Glycine.American journal of human genetics · 2016Article
- An E3-ligase-based method for ablating inhibitory synapses.Nature methods · 2016Article
- Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
shocked (sho) is a zebrafish mutation that causes motor deficits attributable to CNS defects during the first2dof development. Mutant embryos display reduced spontaneous coiling of the trunk, diminished escape responses when touched, and an absence of swimming. A missense mutation in the slc6a9 gene that encodes a glycine transporter (GlyT1) was identified as the cause of the sho phenotype. Antisense knock-down of GlyT1 in wild-type embryos phenocopies sho, and injection of wild-type GlyT1 mRNA into mutants rescues them. A comparison of glycine-evoked inward currents in Xenopus oocytes expressing either the wild-type or mutant protein found that the missense mutation results in a nonfunctional transporter. glyt1 and the related glyt2 mRNAs are expressed in the hindbrain and spinal cord in nonoverlapping patterns. The fact that these regions are known to be required for generation of early locomotory behaviors suggests that the regulation of extracellular glycine levels in the CNS is important for proper function of neural networks. Furthermore, physiological analysis after manipulation of glycinergic activity in wild-type and sho embryos suggests that the mutant phenotype is attributable to elevated extracellular glycine within the CNS.
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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.