ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
The transporters GlyT2 and VIAAT cooperate to determine the vesicular glycinergic phenotype.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 103 citations in OpenAlex.
- SynaptoTagMe, a toolkit for in vivo mapping and modulating neurotransmission at single-cell resolution.eLife · 2026Article
- The sympathoregulatory region of the mouse rostral brainstem relies on both GABA and glycine to generate inhibitory currents.The Journal of physiology · 2026Article
- Dysmorphic neurons express markers of inhibitory glycinergic signaling in focal cortical dysplasia IIb.Brain pathology (Zurich, Switzerland) · 2026Article
- Vesicle docking and fusion pore modulation by the neuronal calcium sensor Synaptotagmin-1.Biophysical journal · 2025Article
- Robust inhibitory glycinergic transmission and the effect of bafilomycin, folimycin and EIPA: lessons from the auditory brainstem.Frontiers in cellular neuroscience · 2025Article
- A neurotransmitter atlas ofeLife · 2024Article
- Vesicle docking and fusion pore modulation by the neuronal calcium sensor Synaptotagmin-1.bioRxiv : the preprint server for biology · 2024Article
- A neurotransmitter atlas ofbioRxiv : the preprint server for biology · 2024Article
- Bidirectional Modulation of Nociception by GlyT2eNeuro · 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
- Glycine-induced NMDA receptor internalization provides neuroprotection and preserves vasculature following ischemic stroke.iScience · 2022Article
- Identification of amacrine neurons with a glycinergic and GABAergic phenotype in the mouse retina.Medical research archives · 2022Article
- Neurotransmitter content heterogeneity within an interneuron class shapes inhibitory transmission at a central synapse.Frontiers in cellular neuroscience · 2022Article
- Article
- Advances in hyperekplexia and other startle syndromes.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Review
- Inhibition of Glycine Re-Uptake: A Potential Approach for Treating Pain by Augmenting Glycine-Mediated Spinal Neurotransmission and Blunting Central Nociceptive Signaling.Biomolecules · 2021Review
- Functional and Biochemical Consequences of Disease Variants in Neurotransmitter Transporters: A Special Emphasis on Folding and Trafficking Deficits.Pharmacology & therapeutics · 2021Review
- Article
- A System for Assessing Dual Action Modulators of Glycine Transporters and Glycine Receptors.Biomolecules · 2020Article
- Neurotransmitter- and Release-Mode-Specific Modulation of Inhibitory Transmission by Group I Metabotropic Glutamate Receptors in Central Auditory Neurons of the Mouse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms that specify the vesicular phenotype of inhibitory interneurons in vertebrates are poorly understood because the two main inhibitory transmitters, glycine and GABA, share the same vesicular inhibitory amino acid transporter (VIAAT) and are both present in neurons during postnatal development. We have expressed VIAAT and the plasmalemmal transporters for glycine and GABA in a neuroendocrine cell line and measured the quantal release of glycine and GABA using a novel double-sniffer patch-clamp technique. We found that glycine is released from vesicles when VIAAT is coexpressed with either the neuronal transporter GlyT2 or the glial transporter GlyT1. However, GlyT2 was more effective than GlyT1, probably because GlyT2 is unable to operate in the reverse mode, which gives it an advantage in maintaining the high cytosolic glycine concentration required for efficient vesicular loading by VIAAT. The vesicular inhibitory phenotype was gradually altered from glycinergic to GABAergic through mixed events when GABA is introduced into the secretory cell and competes for uptake by VIAAT. Interestingly, the VIAAT ortholog from Caenorhabditis elegans (UNC-47), a species lacking glycine transmission, also supports glycine exocytosis in the presence of GlyT2, and a point mutation of UNC-47 that abolishes GABA transmission in the worm confers glycine specificity. Together, these results suggest that an increased cytosolic availability of glycine in VIAAT-containing terminals was crucial for the emergence of glycinergic transmission in vertebrates.
Indexed as
Identifiers
What OpenQuestion holds
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.