A neuroprotective role for microRNA miR-1000 mediated by limiting glutamate excitotoxicity

Nat Neurosci. 2015 Mar;18(3):379-85. doi: 10.1038/nn.3935. Epub 2015 Feb 2.

Abstract

Evidence has begun to emerge for microRNAs as regulators of synaptic signaling, specifically acting to control postsynaptic responsiveness during synaptic transmission. In this report, we provide evidence that Drosophila melanogaster miR-1000 acts presynaptically to regulate glutamate release at the synapse by controlling expression of the vesicular glutamate transporter (VGlut). Genetic deletion of miR-1000 led to elevated apoptosis in the brain as a result of glutamatergic excitotoxicity. The seed-similar miR-137 regulated VGluT2 expression in mouse neurons. These conserved miRNAs share a neuroprotective function in the brains of flies and mice. Drosophila miR-1000 showed activity-dependent expression, which might serve as a mechanism to allow neuronal activity to fine-tune the strength of excitatory synaptic transmission.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Age Factors
  • Aging / genetics
  • Animals
  • Animals, Genetically Modified
  • Cells, Cultured
  • Drosophila
  • Drosophila Proteins / genetics
  • Embryo, Mammalian
  • Embryo, Nonmammalian
  • Female
  • Gene Deletion
  • Gene Expression Regulation, Developmental / genetics*
  • Humans
  • Male
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Neurodegenerative Diseases / genetics
  • Neurodegenerative Diseases / prevention & control*
  • Synaptic Transmission / drug effects
  • Synaptic Transmission / genetics
  • Vesicular Glutamate Transport Protein 2 / genetics
  • Vesicular Glutamate Transport Protein 2 / metabolism

Substances

  • Drosophila Proteins
  • MIRN100 microRNA, Drosophila
  • MicroRNAs
  • Mirn100 microRNA, mouse
  • Slc17a6 protein, mouse
  • Vesicular Glutamate Transport Protein 2