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Synaptopodin is regulated by aromatase activity.

Lars Fester1, Lepu Zhou1, Christiana Ossig1

  • 1Institute of Neuroanatomy, University Medical Center, Hamburg, Germany.

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|November 19, 2016
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Summary

Estrogen synthesis via aromatase (an enzyme) and calcium signaling in the hippocampus regulate synaptic plasticity. This study reveals a novel on-site mechanism involving calcium transients controlling aromatase activity and synaptopodin expression in both sexes.

Keywords:
aromatasecalcium transientsspine apparatusspine synapsessynaptopodin

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Molecular Biology

Background:

  • Locally synthesized estradiol is crucial for hippocampal synaptic plasticity.
  • Aromatase enzyme activity, converting testosterone to estradiol, is regulated by calcium-dependent phosphorylation.
  • Synaptopodin, an estrogen-responsive protein, modulates synaptic plasticity via calcium stores.

Purpose of the Study:

  • To investigate the role of calcium signaling in regulating aromatase activity and synaptopodin expression in the hippocampus.
  • To determine if this regulation is sex-dependent and contributes to synaptic plasticity.

Main Methods:

  • Utilized aromatase inhibitors (letrozole) and knockout mice models.
  • Employed primary-dissociated hippocampal neurons for calcium signaling experiments.
  • Assessed synaptopodin expression via immunohistochemistry and analyzed calcium dynamics.

Main Results:

  • Synaptopodin expression is higher in female hippocampi but downregulated by aromatase phosphorylation in both sexes.
  • Aromatase knockout mice exhibit reduced synaptopodin expression independently of sex.
  • Hippocampal calcium release downregulates aromatase activity and synaptopodin expression, a process disrupted when calcium transients' control over aromatase is impaired.

Conclusions:

  • Neuronal calcium transients regulate hippocampal aromatase activity, influencing synaptopodin expression.
  • This calcium-dependent regulation of aromatase serves as an on-site mechanism impacting synaptic plasticity in both male and female animals.