ArticleFrontiers in molecular neuroscience2009
Defective glycinergic synaptic transmission in zebrafish motility mutants.
Article in Frontiers in molecular neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- A Critical Review of Zebrafish Neurological Disease Models-1. The Premise: Neuroanatomical, Cellular and Genetic Homology and Experimental Tractability.Oxford open neuroscience · 2023Article
- Flux coupling, not specificity, shapes the transport and phylogeny of SLC6 glycine transporters.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- A Great Catch for Investigating Inborn Errors of Metabolism-Insights Obtained from Zebrafish.Biomolecules · 2020Review
- Mitochondria in Embryogenesis: An Organellogenesis Perspective.Frontiers in cell and developmental biology · 2019Article
- Investigation of hindbrain activity during active locomotion reveals inhibitory neurons involved in sensorimotor processing.Scientific reports · 2018Article
- Structure/Function Studies of the α4 Subunit Reveal Evolutionary Loss of a GlyR Subtype Involved in Startle and Escape Responses.Frontiers in molecular neuroscience · 2018Article
- Characterization of the Zebrafish Glycine Receptor Family Reveals Insights Into Glycine Receptor Structure Function and Stoichiometry.Frontiers in molecular neuroscience · 2018Article
- An E3-ligase-based method for ablating inhibitory synapses.Nature methods · 2016Article
- Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016Review
- Distinct phenotypes in zebrafish models of human startle disease.Neurobiology of disease · 2013Article
- Microarray gene expression profiling of neural tissues in bovine spastic paresis.BMC veterinary research · 2013Article
- Behavioral genetics in larval zebrafish: learning from the young.Developmental neurobiology · 2012Review
- Rbfox-regulated alternative splicing is critical for zebrafish cardiac and skeletal muscle functions.Developmental biology · 2011Article
- Duplicated gephyrin genes showing distinct tissue distribution and alternative splicing patterns mediate molybdenum cofactor biosynthesis, glycine receptor clustering, and escape behavior in zebrafish.The Journal of biological chemistry · 2011Article
- Frontiers in molecular neuroscience - résumé and perspective.Frontiers in molecular neuroscience · 2011Article
- Glycinergic transmission: physiological, developmental and pathological implications.Frontiers in molecular neuroscience · 2010Article
- The glycinergic system in human startle disease: a genetic screening approach.Frontiers in molecular neuroscience · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Glycine is a major inhibitory neurotransmitter in the spinal cord and brainstem. Recently, in vivo analysis of glycinergic synaptic transmission has been pursued in zebrafish using molecular genetics. An ENU mutagenesis screen identified two behavioral mutants that are defective in glycinergic synaptic transmission. Zebrafish bandoneon (beo) mutants have a defect in glrbb, one of the duplicated glycine receptor (GlyR) beta subunit genes. These mutants exhibit a loss of glycinergic synaptic transmission due to a lack of synaptic aggregation of GlyRs. Due to the consequent loss of reciprocal inhibition of motor circuits between the two sides of the spinal cord, motor neurons activate simultaneously on both sides resulting in bilateral contraction of axial muscles of beo mutants, eliciting the so-called 'accordion' phenotype. Similar defects in GlyR subunit genes have been observed in several mammals and are the basis for human hyperekplexia/startle disease. By contrast, zebrafish shocked (sho) mutants have a defect in slc6a9, encoding GlyT1, a glycine transporter that is expressed by astroglial cells surrounding the glycinergic synapse in the hindbrain and spinal cord. GlyT1 mediates rapid uptake of glycine from the synaptic cleft, terminating synaptic transmission. In zebrafish sho mutants, there appears to be elevated extracellular glycine resulting in persistent inhibition of postsynaptic neurons and subsequent reduced motility, causing the 'twitch-once' phenotype. We review current knowledge regarding zebrafish 'accordion' and 'twitch-once' mutants, including beo and sho, and report the identification of a new alpha2 subunit that revises the phylogeny of zebrafish GlyRs.
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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.