QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, September 12, 2007, 27(37):9941-9950; doi:10.1523/JNEUROSCI.1647-07.2007

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Related articles in J. Neurosci. Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Boulware, M. I. Articles by Mermelstein, P. G. Search for Related Content PubMed PubMed Citation Articles by Boulware, M. I. Articles by Mermelstein, P. G. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB ESTRADIOL

 Previous Article  |  Next Article 

Cellular/Molecular
Caveolin Proteins Are Essential for Distinct Effects of Membrane Estrogen Receptors in Neurons

Marissa I. Boulware, ^* Holly Kordasiewicz, ^* and Paul G. Mermelstein

Department of Neuroscience, University of Minnesota, Minneapolis, Minnesota 55455

Correspondence should be addressed to Dr. Paul G. Mermelstein, Department of Neuroscience, University of Minnesota, 6-145 Jackson Hall, 321 Church Street Southeast, Minneapolis, MN 55455. Email: pmerm{at}umn.edu

It has become widely accepted that along with its ability to directly regulate gene expression, estradiol also influences cell signaling and brain function via rapid membrane-initiated events. Many of these novel signaling processes are dependent on estrogen receptors (ERs) localized to the neuronal membrane. However, the mechanism(s) by which ERs are able to trigger cell signaling when targeted to the neuronal membrane surface has yet to be determined. In hippocampal neurons, we find that caveolin proteins are essential for the regulation of CREB (cAMP response element-binding protein) phosphorylation after estradiol activation of metabotropic glutamate receptor (mGluR) signaling. Furthermore, caveolin-1 (CAV1) and CAV3 differentially regulate the ability of estradiol to activate two discrete signaling pathways. ER activation of mGluR1a is dependent on CAV1, whereas CAV3 is necessary for ER and ERß activation of mGluR2/3. These results are consistent with previous reports in non-neuronal cells, implicating the importance of caveolin proteins in rapid estrogen signaling. In addition, the functional isolation of distinct estrogen-sensitive signaling pathways by different caveolin proteins suggests novel mechanisms through which the membrane-initiated effects of estradiol are orchestrated.

Key words: estradiol; metabotropic glutamate receptors; CREB; MAPK; L-type calcium channel; hippocampus

---

Received April 12, 2007; revised July 10, 2007; accepted July 30, 2007.

Correspondence should be addressed to Dr. Paul G. Mermelstein, Department of Neuroscience, University of Minnesota, 6-145 Jackson Hall, 321 Church Street Southeast, Minneapolis, MN 55455. Email: pmerm{at}umn.edu

Related articles in J. Neurosci.:

This Week in The Journal

J. Neurosci. 2007 27: i. [Full Text]  

This article has been cited by other articles:

				S. Bake, L. Ma, and F. Sohrabji Estrogen Receptor-{alpha} Overexpression Suppresses 17{beta}-Estradiol-Mediated Vascular Endothelial Growth Factor Expression and Activation of Survival Kinases Endocrinology, August 1, 2008; 149(8): 3881 - 3889. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help