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Defective glycinergic synaptic transmission in zebrafish motility mutants.

Hirata, H; Carta, E; Yamanaka, I; Harvey, RJ; Kuwada, JY; (2010) Defective glycinergic synaptic transmission in zebrafish motility mutants. Frontiers in Molecular Neuroscience , 8 , Article 26. 10.3389/neuro.02.026.2009. Green open access

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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) β 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 α2 subunit that revises the phylogeny of zebrafish GlyRs.

Type: Article
Title: Defective glycinergic synaptic transmission in zebrafish motility mutants.
Open access status: An open access version is available from UCL Discovery
DOI: 10.3389/neuro.02.026.2009
Publisher version: http://dx.doi.org./10.3389/neuro.02.026.2009
Language: English
Additional information: © 2010 Hirata, Carta, Yamanaka, Harvey and Kuwada. This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation. This document is protected by copyright and was first published by Frontiers. All rights reserved. It is reproduced with permission.
Keywords: glycine, synapse, receptor, transporter, zebrafish, behavior, motility
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Life Sciences > UCL School of Pharmacy
URI: http://discovery.ucl.ac.uk/id/eprint/1351321
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