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MicroRNA-137 Controls AMPA-Receptor-Mediated Transmission and mGluR-Dependent LTD

Nikkie F M Olde Loohuis1, Wei Ba2, Peter H Stoerchel3

  • 1Department of Cognitive Neuroscience, Radboudumc, 6500 HB Nijmegen, the Netherlands; Donders Institute for Brain, Cognition, and Behaviour, Centre for Neuroscience, 6525 AJ Nijmegen, the Netherlands.

Cell Reports
|June 23, 2015
PubMed

Insights

MicroRNA miR-137 regulates synaptic transmission by targeting GluA1 AMPA receptors. Its downregulation enhances synaptic efficacy, while overexpression silences synapses, impacting cognitive functions.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Mutations in microRNA miR-137 are linked to cognitive disorders like intellectual disability and schizophrenia.
  • The precise role of miR-137 in brain function and disease pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the direct molecular targets and synaptic functions of microRNA miR-137.
  • To elucidate the role of miR-137 in regulating synaptic plasticity and its connection to glutamatergic signaling.

Main Methods:

  • Bioinformatic analysis to identify miR-137 binding sites on target mRNAs.
  • Experimental validation of GluA1 as a direct miR-137 target.
  • Electrophysiological recordings in hippocampal slices to assess synaptic transmission and plasticity.
  • Manipulation of miR-137 levels in neurons.

Main Results:

  • A conserved miR-137 binding site was identified in the mRNA of GluA1, a subunit of AMPA-type glutamate receptors (AMPARs), confirming GluA1 as a direct target.
  • Downregulation of miR-137 at hippocampal synapses enhanced AMPAR-mediated transmission and activated silent synapses.
  • Overexpression of miR-137 reduced AMPAR transmission and silenced active synapses.
  • miR-137 was transiently upregulated by metabotropic glutamate receptor 5 (mGluR5) activation, and its inhibition impaired mGluR-dependent long-term depression (LTD).

Conclusions:

  • MicroRNA miR-137 plays a critical role in controlling synaptic efficacy and regulating mGluR-dependent synaptic plasticity.
  • Dysregulation of miR-137 and subsequent glutamatergic dysfunction may contribute to the cognitive impairments associated with miR-137-related disorders.

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