Co-expression of VGLUT1 and VGAT sustains glutamate and GABA co-release and is regulated by activity in cortical neurons

Research output: Contribution to journalArticle

Abstract

In adult neocortex, VGLUT1 (also known as SLC17A7), the main glutamate vesicular transporter, and VGAT (also known as SLC32A1), the c-aminobutyric acid (GABA) vesicular transporter, are co-expressed in a subset of axon terminals forming both symmetric and asymmetric synapses, where they are sorted into the same vesicles. However, the functional consequence of this colocalization in cortical neurons has not been clarified. Here, we tested the hypothesis that cortical axon terminals co-expressing VGLUT1 and VGAT can evoke simultaneously monosynaptic glutamate and GABA responses, and investigated whether the amount of terminals co-expressing VGLUT1 and VGAT is affected by perturbations of excitation-inhibition balance. In rat primary cortical neurons, we found that a proportion of synaptic and autaptic responses were indeed sensitive to consecutive application of selective glutamate and GABAA receptor blockers. These 'mixed' synapses exhibited paired-pulse depression. Notably, reducing the activity of the neuronal network by treatment with glutamate receptor antagonists decreased the amount of 'mixed' synapses, whereas reducing spontaneous inhibition by treatment with bicuculline increased them. These synapses might contribute to homeostatic regulation of excitation-inhibition balance.

Original languageEnglish
Pages (from-to)1669-1673
Number of pages5
JournalJournal of Cell Science
Volume128
Issue number9
DOIs
Publication statusPublished - 2015

Keywords

  • Co-release
  • GABA
  • Glutamate
  • VGAT
  • VGLUT1

ASJC Scopus subject areas

  • Cell Biology
  • Medicine(all)

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