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

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

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1] Institute of Molecular and Cell Biology, Singapore. [2] Department of Biological Sciences, National University of Singapore, Singapore.
1] Institute of Molecular and Cell Biology, Singapore. [2] Duke-NUS Graduate Medical School, Singapore. [3] Center for Functional Connectomics, Korea Institute of Science and Technology, Seoul, Republic of Korea. [4] Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore.
1] Warwick-Nanyang Technological University Neuroscience Programme, School of Biological Sciences, Nanyang Technological University, Singapore. [2] School of Life Sciences, University of Warwick, Coventry, UK.


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.

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