𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Selective estrogen receptor-α but not -β agonist treatment modulates brain α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors

✍ Scribed by Maryvonne Le Saux; Erika Estrada-Camarena; Thérèse Di Paolo


Publisher
John Wiley and Sons
Year
2006
Tongue
English
Weight
372 KB
Volume
84
Category
Article
ISSN
0360-4012

No coin nor oath required. For personal study only.

✦ Synopsis


Abstract

Estradiol was previously reported to decrease brain α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazoleproprionic acid (AMPA)‐receptor‐specific binding. The contributions of estrogen receptor subtypes in the estradiol modulation of AMPA receptors and its predominant subunit GluR2 are unknown. These experiments investigated whether an estrogenic receptor subtype is involved in the estradiol effect on AMPA‐receptor‐specific binding and GluR2 mRNA levels. Ovariectomized Sprague‐Dawley rats were treated 2 days after ovariectomy for 2 weeks with 17β‐estradiol, an agonist for ERα 4,4′,4′′‐(4‐propyl‐[1H]‐pyrazole‐1,3,5‐triyl)trisphenol (PPT), or an agonist for ERβ 2,3‐bis(4‐hydroxyphenyl)‐propionitrile (DPN) and compared with intact control rats. Uterus weights, used as aperipheral measure of estrogenic activity, were decreased after ovariectomy and increased by estradiol and PPT but not DPN treatments. In prefrontal and cingulate cortices, the striatum, and the nucleus accumbens, ovariectomy increased [^3^H]AMPA‐specific binding compared with intact controls, which was corrected by estradiol treatment. In all these brain regions, PPT, but not DPN, mimicked the estradiol decrease of AMPA‐receptor‐specific binding; in the cingulate cortex, the effect of PPT did not reach statistical significance. GluR2 mRNA levels of vehicle‐treated ovariectomized rats remained unchanged compared with intact rats in the brain regions investigated. Estradiol and PPT treatment but not DPN decreased GluR2 subunit mRNA levels in the prefrontal cortex and the striatum of ovariectomized rats, whereas no significant change was observed in the cingulate cortex or the nucleus accumbens. The present results suggest that an ERα is involved in the estradiol modulation of AMPA receptors in the cortex, striatum, and nucleus accumbens. © 2006 Wiley‐Liss, Inc.


📜 SIMILAR VOLUMES


α-amino-3-hydroxy-5-methyl-4-isoxazolepr
✍ Alejandro Millán; José Antonio Arias-Montaño; J. Alfredo Méndez; L. Clara R. Her 📂 Article 📅 2004 🏛 John Wiley and Sons 🌐 English ⚖ 481 KB

## Abstract Glutamate, the major excitatory neurotransmitter, induces a wide array of signals from the membrane to the nucleus regulating gene expression. In Bergmann glia, Ca^2+^‐permeable α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole‐ propionic acid (AMPA) receptors are involved in the short‐ and long‐t

New role for spinal Stargazin in α-amino
✍ Feng Tao; John Skinner; Qingning Su; Roger A. Johns 📂 Article 📅 2006 🏛 John Wiley and Sons 🌐 English ⚖ 217 KB 👁 1 views

## Abstract Considerable evidence has demonstrated that α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) receptor blockade has an antinociceptive effect on inflammatory pain. Stargazin (STG) is the first transmembrane protein known to associate with AMPA receptors and regulate their syna

Development of calcium-permeable α-amino
✍ Jette B. Jensen; Arne Schousboe; Darryl S. Pickering 📂 Article 📅 1998 🏛 John Wiley and Sons 🌐 English ⚖ 645 KB

The developmental expression of calcium (Ca2+)-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate receptors in cultured neocortical neurons was evaluated by using cobalt uptake, a histochemical method that identifies cells expressing Ca2+-permeable, non-N-methyl-D-

Compensation by reduced L-α-amino-3-hydr
✍ Tommi P. Möykkynen; Saku T. Sinkkonen; Esa R. Korpi 📂 Article 📅 2007 🏛 John Wiley and Sons 🌐 English ⚖ 110 KB

## Abstract L‐α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) receptor antagonists increase the threshold for electroshock‐induced convulsions. Here, we show that a transgenic mouse line overexpressing cerebellum‐restricted γ‐aminobutyric acid type A (GABA~A~) receptor α6 subunit in the