ArticleFrontiers in synaptic neuroscience2015
Co-release of glutamate and GABA from single vesicles in GABAergic neurons exogenously expressing VGLUT3.
Article in Frontiers in synaptic neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Brain-wide spatiotemporal mapping of glutamate/GABA dual-transmitter neurons during postnatal development in mice.Cell & bioscience · 2026Article
- Circuit-specific remodeling of synaptic co-transmission in stress-responsive networks.Animal cells and systems · 2026Review
- Widespread co-release of glutamate and GABA throughout the mouse brain.Communications biology · 2024Article
- Prevalent co-release of glutamate and GABA throughout the mouse brain.bioRxiv : the preprint server for biology · 2024Article
- Review
- Mixed Excitatory and Inhibitory Projections from the Basolateral Amygdala to the Mediodorsal Thalamic Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- In Vitro Modeling as a Tool for Testing Therapeutics for Spinal Muscular Atrophy and IGHMBP2-Related Disorders.Biology · 2023Article
- A conserved transcriptional fingerprint of multi-neurotransmitter neurons necessary for social behavior.BMC genomics · 2022Article
- A New Player in the Hippocampus: A Review on VGLUT3+ Neurons and Their Role in the Regulation of Hippocampal Activity and Behaviour.International journal of molecular sciences · 2022Review
- Analytical approaches to examine gamma-aminobutyric acid and glutamate vesicular co-packaging.Frontiers in synaptic neuroscience · 2022Review
- Encephalitis patient-derived monoclonal GABAA receptor antibodies cause epileptic seizures.The Journal of experimental medicine · 2021Article
- Article
- Autaptic Cultures: Methods and Applications.Frontiers in synaptic neuroscience · 2020Article
- N-methyl-D-aspartate receptor dysfunction by unmutated human antibodies against the NR1 subunit.Annals of neurology · 2019Article
- Role for VGLUT2 in selective vulnerability of midbrain dopamine neurons.The Journal of clinical investigation · 2018Article
- Contribution of Vesicular Glutamate Transporters to Stress Response and Related Psychopathologies: Studies in VGluT3 Knockout Mice.Cellular and molecular neurobiology · 2018Review
- Glutamate Cotransmission in Cholinergic, GABAergic and Monoamine Systems: Contrasts and Commonalities.Frontiers in neural circuits · 2018Review
- Differential pH Dynamics in Synaptic Vesicles From Intact Glutamatergic and GABAergic Synapses.Frontiers in synaptic neuroscience · 2018Article
- Segregation of glutamatergic and cholinergic transmission at the mixed motoneuron Renshaw cell synapse.Scientific reports · 2017Article
- Hypoxia Stress Modifies NaJournal of experimental neuroscience · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The identity of the vesicle neurotransmitter transporter expressed by a neuron largely corresponds with the primary neurotransmitter that cell releases. However, the vesicular glutamate transporter subtype 3 (VGLUT3) is mainly expressed in non-glutamatergic neurons, including cholinergic, serotonergic, or GABAergic neurons. Though a functional role for glutamate release from these non-glutamatergic neurons has been demonstrated, the interplay between VGLUT3 and the neuron's characteristic neurotransmitter transporter, particularly in the case of GABAergic neurons, at the synaptic and vesicular level is less clear. In this study, we explore how exogenous expression of VGLUT3 in striatal GABAergic neurons affects the packaging and release of glutamate and GABA in synaptic vesicles (SVs). We found that VGLUT3 expression in isolated, autaptic GABAergic neurons leads to action potential evoked release of glutamate. Under these conditions, glutamate and GABA could be packaged together in single vesicles release either spontaneously or asynchronously. However, the presence of glutamate in GABAergic vesicles did not affect uptake of GABA itself, suggesting a lack of synergy in vesicle filling for these transmitters. Finally, we found postsynaptic detection of glutamate released from GABAergic terminals difficult when bona fide glutamatergic synapses were present, suggesting that co-released glutamate cannot induce postsynaptic glutamate receptor clustering.
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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.