Evidence map›Paper›PMID 21205416›Full record

ArticleThe international journal of neuropsychopharmacology2011

Corticotropin-releasing factor and noradrenergic signalling exert reciprocal control over startle reactivity.

Jodi E Gresack, Victoria B Risbrough

Open access · bronzeAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2011. 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
0.8field-weighted citation impact, top 36% 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, 28 citations in OpenAlex.

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  12. Generation and characterization of humanized mice carrying COMT158 Met/Val alleles.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014
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  15. Corticotropin-releasing factor acting at the locus coeruleus disrupts thalamic and cortical sensory-evoked responses.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012
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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.

Jodi E GresackDepartment of Psychiatry, University of California, San Diego, La Jolla, CA 92093-0804, USA.
Victoria B Risbrough
University of California, San Diego · US

Funding

Stress and CRF System Effects on Information ProcessingR01MH074697 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISBROUGH, VICTORIA B · 2006 to 2014
$2.5M
NIMH NIH HHS MH074697NIMH NIH HHS R01 MH074697
6 · The paper itself

Abstract

Corticotropin-releasing factor (CRF) and norepinephrine (NE) levels are altered in post-traumatic stress disorder and may be related to symptoms of hyperarousal, including exaggerated startle, in these patients. In animals, activation of both systems modulates anxiety behaviours including startle plasticity; however, it is unknown if they exert their actions orthogonally or dependently. We tested the hypothesis that NE receptor activation is required for CRF effects on startle and that CRF1 receptor activation is required for NE effects on startle. The study examined the effects of: (1) α2 agonist clonidine (0.18 mg/kg i.p.), α1 antagonist prazosin (0.8 mg/kg), and β1/2 antagonist propranolol (0.8, 8.0 mg/kg) pretreatment on ovine-CRF (oCRF)- (0.6 nmol) induced increases in startle reactivity and disruption of prepulse inhibition (PPI); (2) α2 antagonist atipamezole (1-30 mg/kg) and α1 agonist cirazoline (0.025-1.0 mg/kg) treatment on startle; (3) CRF1 antagonist (antalarmin, 14 mg/kg) pretreatment on atipamezole- (10.0 mg/kg) induced increases in startle. oCRF robustly increased startle and reduced PPI. Pretreatment with clonidine or prazosin, but not propranolol, blocked oCRF-induced increases in startle but had no effect on oCRF-induced disruptions in PPI. Atipamezole treatment increased startle, which was partially attenuated by CRF1 antagonist pretreatment. Cirazoline treatment did not increase startle. These findings suggest that CRF modulation of startle, but not PPI, requires activation of α1 adrenergic receptors, while CRF1 activation also contributes to NE modulation of startle. These data support a bi-directional model of CRF-NE modulation of stress responses and suggest that both systems must be activated to induce stress effects on startle reactivity.

Indexed as

Reflex, StartleSynaptic TransmissionAdrenergic alpha-1 Receptor AntagonistsAdrenergic alpha-2 Receptor AgonistsAdrenergic alpha-2 Receptor AntagonistsAnimalsBehavior, AnimalCerebral CortexCorticotropin-Releasing HormoneCRF Receptor, Type 1Infusions, IntraventricularLocus CoeruleusMaleMiceMice, Inbred C57BLNerve Tissue ProteinsAdrenergic alpha-1 Receptor AntagonistsAdrenergic alpha-2 Receptor AgonistsAdrenergic alpha-2 Receptor AntagonistsCorticotropin-Releasing HormoneCRF Receptor, Type 1Nerve Tissue ProteinsNorepinephrineReceptors, AdrenergicReceptors, Corticotropin-Releasing Hormone

Identifiers

PMID21205416
PMCPMC3601827
OpenAlexW2168869903

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.