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MIR137 schizophrenia-associated locus controls synaptic function by regulating synaptogenesis, synapse maturation and

Enqi He1, Miguel A Gonzalez Lozano2, Sven Stringer3

  • 1Department of Functional Genomics, Center for Neurogenomics and Cognitive Research (CNCR), Amsterdam Neuroscience, VU University Amsterdam and VU Medical Center, 1081 HV Amsterdam, The Netherlands.

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The MIR137 gene

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • The MIR137 locus is a known genetic risk factor for schizophrenia.
  • Increased miR-137 expression is associated with the risk allele and affects synaptic transmission.

Purpose of the Study:

  • To investigate the cellular mechanisms by which miR-137 overexpression impacts synaptic function in mouse hippocampal neurons.
  • To correlate the schizophrenia risk allele with gene expression in the MIR137 locus in human brain tissue.

Main Methods:

  • Correlation analysis of MIR137 locus gene expression with the risk allele in human postmortem brain.
  • Experimental manipulation of miR-137 levels in cultured mouse hippocampal neurons.
  • Electrophysiological recordings to assess synaptic transmission.
  • Ultrastructural morphometry to analyze synaptic vesicle dynamics.
  • Proteomic analysis to identify altered protein expression.
  • Synaptogenesis assays to quantify synapse formation.

Main Results:

  • Evidence of increased MIR137HG expression linked to the disease-associated genotype in human hippocampus.
  • miR-137 overexpression reduced evoked and spontaneous synaptic transmission by 50% in mouse neurons, due to defects in release probability.
  • Ultrastructural analysis revealed alterations in docking, active zone length, and vesicle number, but not selective docking defects.
  • Proteomic and immunocytochemistry data showed unaltered Syt1 and Cplx1 levels, contrary to previous reports.
  • Proteomic analysis identified altered expression of synaptogenesis-related genes, with a 31% reduction in synapse formation.

Conclusions:

  • miR-137 regulates synaptic function through modulation of synaptogenesis, synaptic ultrastructure, and overall synapse function.
  • These miR-137-mediated effects on synaptic mechanisms are plausible contributors to the increased schizophrenia risk observed with miR-137 overexpression.