Evidence map›Paper›PMID 11394633›Full record

ArticleEndocrine2001

Receptor phosphorylation mediates estradiol reduction of alpha2-adrenoceptor coupling to G protein in the hypothalamus of female rats.

M A Ansonoff, A M Etgen

Abstract read
PubMed Publisher
In one paragraph

Article in Endocrine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 29 citations in OpenAlex.

  1. Effects of fadolmidine, an αPharmacology research & perspectives · 2021
    Article
  2. Article
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  4. Article
  5. Menopausal hot flashes: mechanisms, endocrinology, treatment.The Journal of steroid biochemistry and molecular biology · 2014
    Review
  6. Article
  7. Article
  8. Article
  9. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

M A AnsonoffDepartment of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
A M Etgen
Albert Einstein College of Medicine · US

Funding

NEUROENDOCRINE BASES OF REPRODUCTIVE BEHAVIORR01HD029856 · NICHD · YESHIVA UNIVERSITY · PI ETGEN, ANNE M · 1993 to 2006
$2.3M
NEUROENDOCRINE REGULATION OF BEHAVIORK02MH000636 · NIMH · YESHIVA UNIVERSITY · PI ETGEN, ANNE M · 1986 to 1995
–
AGING TRAINING GRANTT32AG000194 · NIA · YESHIVA UNIVERSITY · PI HAMERMAN, DAVID · 1989 to 1998
–
NIA NIH HHS T32 AG-00194NICHD NIH HHS HD-29856NIMH NIH HHS MH-00636
6 · The paper itself

Abstract

Estrogen increases evoked norepinephrine release in the hypothalamus of female rodents, in part by reducing the ability of alpha2-adrenoceptors to act as negative feed-back inhibitors of norepinephrine release. Estrogen enhancement of norepinephrine release in the hypothalamus correlates with decreased coupling of the alpha2-adrenoceptor to G protein. To determine the mechanism by which estrogen uncouples alpha2-adrenoceptors from G protein, we tested the hypothesis that estrogen increases alpha2-adrenoceptor phosphorylation. Short-term activation of endogenous serine/threonine phosphatases with protamine or treatment with exogenous phosphatase restored alpha2-adrenoceptor coupling to G protein to control levels in hypothalami from estrogen-exposed female rats. Additional experiments examined whether estrogen alters G protein-coupled receptor kinase expression or activity or serine/threonine phosphatase activity. These proteins are involved in G protein-coupled receptor phosphorylation, internalization, and recycling. Estrogen exposure reduced G protein-coupled receptor kinase mRNA, protein, and activity in the hypothalamus. Furthermore, estrogen treatment reduced serine/threonine phosphatase activity in the hypothalamus. Analysis of ligand binding in subcellular fractions demonstrated that estrogen decreases the fraction of internalized alpha2-adrenoceptors in the hypothalamus.Therefore, estrogen promotes norepinephrine release in the hypothalamus by stabilizing alpha2-adrenoceptor phosphorylation, uncoupling the receptor from G protein. Estrogen may stabilize alpha2-adrenoceptor phosphorylation by inhibiting receptor internalization and dephosphorylation.

Indexed as

Adrenergic alpha-AntagonistsAnimalsbeta-Adrenergic Receptor KinasesCell MembraneCyclic AMP-Dependent Protein KinasesEnzyme ActivationEstradiolFemaleGene ExpressionGTP-Binding ProteinsHypothalamusIdazoxanNorepinephrineOvariectomyPhosphoprotein PhosphatasesPhosphorylation2-methoxyidazoxanAdrenergic alpha-Antagonistsbeta-Adrenergic Receptor KinasesCyclic AMP-Dependent Protein KinasesEstradiolGTP-Binding ProteinsIdazoxanNorepinephrinePhosphoprotein PhosphatasesReceptors, Adrenergic, alpha-2Tritium

Identifiers

PMID11394633
OpenAlexW2185952464

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.