ArticleThe Journal of physiology2013
Dynamic regulation of glycine-GABA co-transmission at spinal inhibitory synapses by neuronal glutamate transporter.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- The sympathoregulatory region of the mouse rostral brainstem relies on both GABA and glycine to generate inhibitory currents.The Journal of physiology · 2026Article
- GABA corelease guides the functional maturation of glycinergic synapses in an auditory sound localization circuit.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Pleiotropic neurotransmitters: neurotransmitter-receptor crosstalk regulates excitation-inhibition balance in social brain functions and pathologies.Frontiers in neuroscience · 2025Review
- Interactions Involving Glycine and Other Amino Acid Neurotransmitters: Focus on Transporter-Mediated Regulation of Release and Glycine-Glutamate Crosstalk.Biomedicines · 2024Review
- Glutamate Spillover Dynamically Strengthens Gabaergic Synaptic Inhibition of the Hypothalamic Paraventricular Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Chronic intermittent hypoxia enhances glycinergic inhibition in nucleus tractus solitarius.Journal of neurophysiology · 2022Article
- Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord.International journal of molecular sciences · 2022Review
- Neurotransmitter content heterogeneity within an interneuron class shapes inhibitory transmission at a central synapse.Frontiers in cellular neuroscience · 2022Article
- Glycine Signaling in the Framework of Dopamine-Glutamate Interaction and Postsynaptic Density. Implications for Treatment-Resistant Schizophrenia.Frontiers in psychiatry · 2020Review
- GABA is a modulator, rather than a classical transmitter, in the medial nucleus of the trapezoid body-lateral superior olive sound localization circuit.The Journal of physiology · 2019Article
- Expression of functional inhibitory neurotransmitter transporters GlyT1, GAT-1, and GAT-3 by astrocytes of inferior colliculus and hippocampus.Molecular brain · 2018Article
- Heterogeneous Signaling at GABA and Glycine Co-releasing Terminals.Frontiers in synaptic neuroscience · 2018Article
- Corelease of Inhibitory Neurotransmitters in the Mouse Auditory Midbrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Caloric restriction selectively reduces the GABAergic phenotype of mouse hypothalamic proopiomelanocortin neurons.The Journal of physiology · 2017Article
- Developmental Shift of Inhibitory Transmitter Content at a Central Auditory Synapse.Frontiers in cellular neuroscience · 2017Article
- Gad1 mRNA as a reliable indicator of altered GABA release from orexigenic neurons in the hypothalamus.The European journal of neuroscience · 2015Article
- A Transgenic Mouse Line Expressing the Red Fluorescent Protein tdTomato in GABAergic Neurons.PloS one · 2015Article
- Dual-transmitter neurons: functional implications of co-release and co-transmission.Current opinion in neurobiology · 2014Review
- Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fast inhibitory neurotransmission in the central nervous system is mediated by γ-aminobutyric acid (GABA) and glycine, which are accumulated into synaptic vesicles by a common vesicular inhibitory amino acid transporter (VIAAT) and are then co-released. However, the mechanisms that control the packaging of GABA + glycine into synaptic vesicles are not fully understood. In this study, we demonstrate the dynamic control of the GABA-glycine co-transmission by the neuronal glutamate transporter, using paired whole-cell patch recording from monosynaptically coupled cultured spinal cord neurons derived from VIAAT-Venus transgenic rats. Short step depolarization of presynaptic neurons evoked unitary (cell-to-cell) inhibitory postsynaptic currents (IPSCs). Under normal conditions, the fractional contribution of postsynaptic GABA or glycine receptors to the unitary IPSCs did not change during a 1 h recording. Intracellular loading of GABA or glycine via a patch pipette enhanced the respective components of inhibitory transmission, indicating the importance of the cytoplasmic concentration of inhibitory transmitters. Raised extracellular glutamate levels increased the amplitude of GABAergic IPSCs but reduced glycine release by enhancing glutamate uptake. Similar effects were observed when presynaptic neurons were intracellularly perfused with glutamate. Interestingly, high-frequency trains of stimulation decreased glycinergic IPSCs more than GABAergic IPSCs, and repetitive stimulation occasionally failed to evoke glycinergic but not GABAergic IPSCs. The present results suggest that the enhancement of GABA release by glutamate uptake may be advantageous for rapid vesicular refilling of the inhibitory transmitter at mixed GABA/glycinergic synapses and thus may help prevent hyperexcitability.
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