ArticleJournal of neurophysiology2008
Synaptic homeostasis in a zebrafish glial glycine transporter mutant.
Article in Journal of neurophysiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Context-dependent hyperactivity inFrontiers in molecular neuroscience · 2024Article
- 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
- Mechanisms underlying homeostatic plasticity in theProceedings of the National Academy of Sciences of the United States of America · 2020Article
- 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
- In Vivo Measurement of Glycine Receptor Turnover and Synaptic Size Reveals Differences between Functional Classes of Motoneurons in Zebrafish.Current biology : CB · 2017Article
- Defects of the Glycinergic Synapse in Zebrafish.Frontiers in molecular neuroscience · 2016Review
- A single mutation in the acetylcholine receptor δ-subunit causes distinct effects in two types of neuromuscular synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Homeostatic synaptic plasticity in developing spinal networks driven by excitatory GABAergic currents.Neuropharmacology · 2014Review
- Defective escape behavior in DEAH-box RNA helicase mutants improved by restoring glycine receptor expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Touch responsiveness in zebrafish requires voltage-gated calcium channel 2.1b.Journal of neurophysiology · 2012Article
- TRPM7 is required within zebrafish sensory neurons for the activation of touch-evoked escape behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Synaptic scaling and the development of a motor network.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Glutamate drives the touch response through a rostral loop in the spinal cord of zebrafish embryos.Developmental neurobiology · 2009Article
- Defective glycinergic synaptic transmission in zebrafish motility mutants.Frontiers in molecular neuroscience · 2009Article
- Glycinergic synapse development, plasticity, and homeostasis in zebrafish.Frontiers in molecular neuroscience · 2009Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Truncated escape responses characteristic of the zebrafish shocked mutant result from a defective glial glycine transporter (GlyT1). In homozygous GlyT1 mutants, irrigating brain ventricles with glycine-free solution rescues normal swimming. Conversely, elevating brain glycine levels restores motility defects. These experiments are consistent with previous studies that demonstrate regulation of global glycine levels in the CNS as a primary function of GlyT1. As GlyT1 mutants mature, their ability to mount an escape response naturally recovers. To understand the basis of this recovery, we assay synaptic transmission in primary spinal motor neurons by measuring stimulus-evoked postsynaptic potentials. At the peak of the motility defect, inhibitory synaptic potentials are both significantly larger and more prolonged indicating a prominent role for GlyT1 in shaping fast synaptic transmission. However, as GlyT1 mutants naturally regain their ability to swim, the amplitude of inhibitory potentials decreases to below wild-type levels. In parallel with diminishing synaptic potentials, the glycine concentration required to evoke the mutant motility defect increases 61-fold during behavioral recovery. Behavioral recovery is also mirrored by a reduction in the levels of both glycine receptor protein and transcript. These results suggest that increased CNS glycine tolerance and reduced glycine receptor expression in GlyT1 mutants reflect compensatory mechanisms for functional recovery from excess nervous system inhibition.
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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.