Evidence map›Paper›PMID 20430865›Full record

ArticleMolecular pharmacology2010

Enhanced hypotensive, bradycardic, and hypnotic responses to alpha2-adrenergic agonists in spinophilin-null mice are accompanied by increased G protein coupling to the alpha2A-adrenergic receptor.

R Lu, Y Chen, C Cottingham, N Peng, K Jiao, L E Limbird, J M Wyss, Q Wang

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Spinophilin-deficient mice are protected from diet-induced obesity and insulin resistance.American journal of physiology. Endocrinology and metabolism · 2020
    Article
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  8. Review
  9. The amyloid precursor protein modulates αFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
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  14. Review
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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

8 authors at 1 institution in 1 country.

R LuDepartment of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Y Chen
C Cottingham
N Peng
K Jiao
L E Limbird
J M Wyss
Q Wang
University of Alabama at Birmingham · US

Funding

Alabama Neuroscience Blueprint Core CenterP30NS057098 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SWEATT, JOHN DAVID · 2006 to 2010
$9.5M
UAB Neuroscience Core CenterP30NS047466 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STANDAERT, DAVID G. · 2005 to 2019
$8.5M
Regulation of novel alpha2A adrenergic receptor signaling by spinophilinR01MH081917 · NIMH · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, QIN · 2009 to 2019
$3.9M
TARGETING ALPHA-2 RECEPTOR TO RENAL BASOLATERAL MEMBRANER01DK043879 · NIDDK · VANDERBILT UNIVERSITY · PI LIMBIRD, LEE E · 1993 to 2004
$1.3M
NIDDK NIH HHS DK43879NIDDK NIH HHS R01 DK043879NIMH NIH HHS MH081917NIMH NIH HHS R01 MH081917NINDS NIH HHS NS047466NINDS NIH HHS NS057098NINDS NIH HHS P30 NS047466NINDS NIH HHS P30 NS057098
6 · The paper itself

Abstract

We previously identified spinophilin as a regulator of alpha(2) adrenergic receptor (alpha(2)AR) trafficking and signaling in vitro and in vivo (Science 304:1940-1944, 2004). To assess the generalized role of spinophilin in regulating alpha(2)AR functions in vivo, the present study examined the impact of eliminating spinophilin on alpha(2)AR-evoked cardiovascular and hypnotic responses, previously demonstrated to be mediated by the alpha(2A)AR subtype, after systemic administration of the alpha(2)-agonists 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine (UK14,304) and clonidine in spinophilin-null mice. Mice lacking spinophilin expression display dramatically enhanced and prolonged hypotensive, bradycardic, and sedative-hypnotic responses to alpha(2)AR stimulation. Whereas these changes in sensitivity to alpha(2)AR agonists occur independent of any changes in alpha(2A)AR density or intrinsic affinity for agonist in the brains of spinophilin-null mice compared with wild-type control mice, the coupling of the alpha(2A)AR to cognate G proteins is enhanced in spinophilin-null mice. Thus, brain preparations from spinophilin-null mice demonstrate enhanced guanine nucleotide regulation of UK14,304 binding and evidence of a larger fraction of alpha(2A)AR in the guanine-nucleotide-sensitive higher affinity state compared with those from wild-type mice. These findings suggest that eliminating spinophilin expression in native tissues leads to an enhanced receptor/G protein coupling efficiency that contributes to sensitization of receptor mediated responses in vivo.

Indexed as

Adrenergic alpha-2 Receptor AgonistsAdrenergic alpha-AgonistsAnimalsBradycardiaGTP-Binding ProteinsHypnotics and SedativesMaleMiceMice, KnockoutMicrofilament ProteinsNerve Tissue ProteinsNeurabinsProtein BindingRadioligand AssayReceptors, Adrenergic, alpha-2Rotarod Performance TestAdrenergic alpha-2 Receptor AgonistsAdrenergic alpha-AgonistsGTP-Binding ProteinsHypnotics and SedativesMicrofilament ProteinsNerve Tissue ProteinsNeurabinsReceptors, Adrenergic, alpha-2

Identifiers

PMID20430865
PMCPMC2917858
OpenAlexW2104819786

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.