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Brain Aromatase, Estrogens, and Behavior$
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Jacques Balthazart and Gregory Ball

Print publication date: 2012

Print ISBN-13: 9780199841196

Published to Oxford Scholarship Online: January 2013

DOI: 10.1093/acprof:oso/9780199841196.001.0001

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Cellular Mechanisms Controlling Rapid Changes in Brain Aromatase Activity

Cellular Mechanisms Controlling Rapid Changes in Brain Aromatase Activity

Chapter:
(p.416) Chapter 22 Cellular Mechanisms Controlling Rapid Changes in Brain Aromatase Activity
Source:
Brain Aromatase, Estrogens, and Behavior
Author(s):

Thierry D. Charlier

Charlotte A. Cornil

Gregory F. Ball

Jacques Balthazart

Publisher:
Oxford University Press
DOI:10.1093/acprof:oso/9780199841196.003.0022

Beside their action at the genomic level, estrogens such as 17β-estradiol (E2) also activate rapid and transient cellular, physiological, and behavioral changes. Aromatase is the key limiting enzyme in the production of estrogens and the rapid modulation of this enzymatic activity could produce rapid changes in local E2 concentrations. The mechanisms that might mediate such rapid enzymatic changes are thus currently under intense scrutiny. Recent studies in our laboratory indicate that brain aromatase activity is rapidly inhibited by an increase in intracellular calcium concentration that results from potassium-induced depolarization or from the activation of glutamatergic receptors. Altogether, the phosphorylation/dephosphorylation processes affecting aromatase activity provide a new general mechanism by which the concentration of estrogens can be rapidly altered in the brain and other tissues.

Keywords:   17β-estradiol, aromatase activity, estrogen receptor alpha, phosphorylation, HEK293, Hypothalamus, Japanese quail

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