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Synaptopodin is regulated by aromatase activity
Lars Fester1, Lepu Zhou1, Christiana Ossig1
1Institute of Neuroanatomy, University Medical Center, Hamburg, Germany.
Journal of Neurochemistry
|November 19, 2016
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.
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.
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