Cited by 89Neuroscience and Neuropharmacology ResearchCellular transport and secretionAmino Acid Enzymes and Metabolism

Activity-dependent regulation of vesicular glutamate and GABA transporters: A means to scale quantal size

Erickson, Jeffrey D., De Gois, Stéphanie, Varoqui, Hélène, Schafer, Martin K.-H., Weihe, Eberhard·2006·Neurochemistry International

Abstract

The functional balance of glutamatergic and GABAergic signaling in neuronal cortical circuits is under homeostatic control. That is, prolonged alterations of global network activity leads to opposite changes in quantal amplitude at glutamatergic and GABAergic synapses. Such scaling of excitatory and inhibitory transmission within cortical circuits serves to restore and maintain a constant spontaneous firing rate of pyramidal neurons. Our recent work shows that this includes alterations in the levels of expression of vesicular glutamate (VGLUT1 and VGLUT2) and GABA (VIAAT) transporters. Other vesicle markers, such as synaptophysin or synapsin, are not regulated in this way. Endogenous regulation at the level of mRNA and synaptic protein controls the number of transporters per vesicle and hence, the level of vesicle filling with transmitter. Bidirectional and opposite activity-dependent regulation of VGLUT1 and VIAAT expression would serve to adjust the balance of glutamate and GABA release and therefore the level of postsynaptic receptor saturation. In some excitatory neurons and synapses, co-expression of VGLUT1 and VGLUT2 occurs. Bidirectional and opposite changes in the levels of two excitatory vesicular transporters would enable individual neocortical neurons to scale up or scale down the level of vesicular glutamate storage, and thus, the amount available for release at individual synapses. Regulated vesicular transmitter storage and release via selective changes in the l…

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Crossref · 10.1016/j.neuint.2005.12.029

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  • Glutamate transporter (VGlut) expression in the presynaptic terminal can be enhanced by activity blockade.

    “For example, there is evidence that glutamate transporter (VGlut) expression in the presynaptic terminal can be enhanced by activity blockade (De Gois et al. 2005;Erickson et al. 2006), raising the possibility that in addition to adding more postsynaptic receptors, neurons might also package more neurotransmitters into each presynaptic vesicle; these two processes would then collaborate to scale”

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References 94 · Cited by 89

Authors
Erickson, J. D., De Gois, S., Varoqui, H., Schafer, M. K.-H., & Weihe, E.
Affiliations
  • Louisiana State University Health Sciences Center New Orleans (US)
  • Philipps University of Marburg (DE)
Corresponding author
Erickson, Jeffrey D.
Venue
Neurochemistry International
Publisher
Elsevier BV
Published
2006-05
Volume
48
Issue
6-7
Pages
643-649
ISSN
0197-0186 (ISSN-L)
OpenAlex
W1974988575
Cited by
89
References
94
Citations by year
2026: 1 · 2024: 1 · 2023: 3 · 2022: 1 · 2021: 4 · 2020: 7 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 5 · 2015: 7 · 2014: 3 · 2013: 4 · 2012: 4
FWCI
3.87
Type
journal article
Language
en
Open access
closed
Locations
  • Neurochemistry International (publishedVersion)
  • PubMed (publishedVersion)
  • HAL (submittedVersion)
Funders
  • Bundesministerium für Bildung und Forschung (01GS01118)
  • National Institutes of Health (1P29RR16816, NS36936)
  • National Alliance for Research on Schizophrenia and Depression
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
Keywords
vesicular glutamate transporter, vesicular GABA transporter, VGLUT1, VGLUT2, activity-dependent regulation, quantal size, synaptic homeostasis, excitation-inhibition balance, neocortical pyramidal neurons, glutamate release, GABA release
MeSH terms
Animals, Cerebral Cortex, Homeostasis, Humans, Nerve Net, Neuronal Plasticity, Neurons, Synapses, Glutamic Acid, Vesicular Inhibitory Amino Acid Transport Proteins, Vesicular Glutamate Transport Protein 1, Vesicular Glutamate Transport Protein 2

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