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

Pushpa Verma; George J Augustine; Mohamed-Raafet Ammar; Ayumu Tashiro; Stephen M Cohen

doi:10.1038/nn.3935

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

Pushpa Verma, George J Augustine, Mohamed-Raafet Ammar, Ayumu Tashiro, Stephen M Cohen

Morphogenesis and Differentiation Program

42 Citationer (Scopus)

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.

Originalsprog	Engelsk
Tidsskrift	Nature Neuroscience
Vol/bind	18
Udgave nummer	3
Sider (fra-til)	379-85
Antal sider	7
ISSN	1097-6256
DOI	https://doi.org/10.1038/nn.3935
Status	Udgivet - 27 mar. 2015

Adgang til dokumentet

10.1038/nn.3935

Citationsformater

@article{8bbd0708560e46ab8e2c39aba3cfd57d,

title = "A neuroprotective role for microRNA miR-1000 mediated by limiting glutamate excitotoxicity",

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.",

author = "Pushpa Verma and Augustine, {George J} and Mohamed-Raafet Ammar and Ayumu Tashiro and Cohen, {Stephen M}",

year = "2015",

month = mar,

day = "27",

doi = "10.1038/nn.3935",

language = "English",

volume = "18",

pages = "379--85",

journal = "Nature Neuroscience",

issn = "1097-6256",

publisher = "nature publishing group",

number = "3",

}

TY - JOUR

T1 - A neuroprotective role for microRNA miR-1000 mediated by limiting glutamate excitotoxicity

AU - Verma, Pushpa

AU - Augustine, George J

AU - Ammar, Mohamed-Raafet

AU - Tashiro, Ayumu

AU - Cohen, Stephen M

PY - 2015/3/27

Y1 - 2015/3/27

N2 - 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.

AB - 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.

U2 - 10.1038/nn.3935

DO - 10.1038/nn.3935

M3 - Journal article

C2 - 25643297

SN - 1097-6256

VL - 18

SP - 379

EP - 385

JO - Nature Neuroscience

JF - Nature Neuroscience

IS - 3

ER -

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

Abstract

Adgang til dokumentet

Fingeraftryk

Citationsformater