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This version published online on September 29, 2005
Endocrinology, doi:10.1210/en.2005-0845
A more recent version of this article appeared on January 1, 2006
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*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*GLUTAMIC ACID HYDROCHLORIDE

Submitted on July 7, 2005
Accepted on September 21, 2005

Rapid Control of Brain Aromatase Activity by Glutamatergic Inputs

Jacques Balthazart*, Michelle Baillien, and Gregory F. Ball

University of Liège, Center for Cellular and Molecular Neurobiology, Research Group in Behavioral Neuroendocrinology, B-4000 Liège 1, Belgium (JB, MB), Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD 21218, USA (GFB)

* To whom correspondence should be addressed. E-mail: jbalthazart{at}ulg.ac.be.

Estrogens derived from the neural aromatization of testosterone play a key role in the activation of male sexual behavior in many vertebrates and have now been recognized to have rapid membrane effects on brain function. Such changes in aromatase activity and hence in local estrogen concentrations could rapidly modulate behavioral responses. We show here that there is a very rapid (within min) decrease in aromatase activity in quail hypothalamic explants exposed to treatments affecting intracellular Ca2+ concentrations such as the addition of glutamate agonists (kainate, AMPA and to a much lesser extent NMDA) but not of GABA. The kainate effects, which reduce aromatase activity by 25-50% are observed within 5 min and completely blocked in explants exposed to specific kainate antagonists (CNQX or NBQX) and are also rapidly reversible when effectors are washed out. Together these data support the notion that the synthesis of estrogen can be rapidly regulated in the brain thus producing rapid changes in local estrogen bioavailability that could rapidly modify brain function with a time-course similar to what has previously been described for neurotransmitters and neuromodulators.


Key words: Aromatase activity • Preoptic area • Coturnix japonica • Fast steroid action • Phosphorylation




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