Evidence map›Paper›PMID 21976502›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Stress and glucocorticoids impair memory retrieval via β2-adrenergic, Gi/o-coupled suppression of cAMP signaling.

Keith Schutsky, Ming Ouyang, Christina B Castelino, Lei Zhang, Steven A Thomas

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Cortisol effects on flow-experience.Psychopharmacology · 2015
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  11. Noradrenergic Modulation of Fear Conditioning and Extinction.Frontiers in behavioral neuroscience · 2018
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Astrocytic β2-adrenergic receptors mediate hippocampal long-term memory consolidation.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  17. Article
  18. Article
  19. 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

5 authors at 1 institution in 1 country.

Keith SchutskyDepartment of Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6084, USA.
Ming Ouyang
Christina B Castelino
Lei Zhang
Steven A Thomas
University of Pennsylvania · US

Funding

PREDOCTORAL TRAINING PROGRAM IN PHARMACOLOGYT32GM008076 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BLENDY, JULIE A · 1985 to 2023
$10.8M
Molecular mechanisms of memrory retrievalR01MH063352 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI THOMAS, STEVEN A · 2002 to 2011
$3.2M
NIGMS NIH HHS 5T32GM008076NIGMS NIH HHS T32 GM008076NIMH NIH HHS 5R01MH063352NIMH NIH HHS R01 MH063352
6 · The paper itself

Abstract

Acute stress impairs the retrieval of hippocampus-dependent memory, and this effect is mimicked by exogenous administration of stress-responsive glucocorticoid hormones. It has been proposed that glucocorticoids affect memory by promoting the release and/or blocking the reuptake of norepinephrine (NE), a stress-responsive neurotransmitter. It has also been proposed that this enhanced NE signaling impairs memory retrieval by stimulating β(1)-adrenergic receptors and elevating levels of cAMP. In contrast, other evidence indicates that NE, β(1), and cAMP signaling is transiently required for the retrieval of hippocampus-dependent memory. To resolve this discrepancy, wild-type rats and mice with and without gene-targeted mutations were stressed or treated with glucocorticoids and/or adrenergic receptor drugs before testing memory for inhibitory avoidance or fear conditioning. Here we report that glucocorticoids do not require NE to impair retrieval. However, stress- and glucocorticoid-induced impairments of retrieval depend on the activation of β(2) (but not β(1))-adrenergic receptors. Offering an explanation for the opposing functions of these two receptors, the impairing effects of stress, glucocorticoids and β(2) agonists on retrieval are blocked by pertussis toxin, which inactivates signaling by G(i/o)-coupled receptors. In hippocampal slices, β(2) signaling decreases cAMP levels and greatly reduces the increase in cAMP mediated by β(1) signaling. Finally, augmenting cAMP signaling in the hippocampus prevents the impairment of retrieval by systemic β(2) agonists or glucocorticoids. These results demonstrate that the β(2) receptor can be a critical effector of acute stress, and that β(1) and β(2) receptors can have quite distinct roles in CNS signaling and cognition.

Indexed as

AnimalsCyclic AMPFearFemaleGlucocorticoidsGTP-Binding Protein alpha Subunits, Gi-GoMaleMemoryMiceMice, 129 StrainMice, Inbred C57BLMice, Inbred DBAMice, KnockoutMice, TransgenicPertussis ToxinRatsCyclic AMPGlucocorticoidsGTP-Binding Protein alpha Subunits, Gi-GoPertussis ToxinReceptors, Adrenergic, beta-2

Identifiers

PMID21976502
PMCPMC3200569
OpenAlexW1978286371

What OpenQuestion holds

Textmetadata
LicenceTDM
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.