Evidence map›Paper›PMID 17989300›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

Noradrenergic modulation of basolateral amygdala neuronal activity: opposing influences of alpha-2 and beta receptor activation.

Deanne M Buffalari, Anthony A Grace

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Pooled it
  2. Guanfacine modulates the emotional biasing of amygdala-prefrontal connectivity for cognitive control.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2014
    Trial
  3. Trial
  4. Noradrenergic enhancement of amygdala responses to fear.Social cognitive and affective neuroscience · 2009
    Trial
  5. Review
  6. Sequential decreases in basolateral amygdala response to threat predict failure to recover from PTSD.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Identification of a stress-responsive subregion of the basolateral amygdala in male rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

25 more citing papers are in PubMed but not listed here.

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.

Deanne M BuffalariDepartment of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260, USA.
Anthony A Grace
University of Pittsburgh · US

Funding

Stress-Induced Alterations in Amygdala-LC InteractionsR01DA015408 · NIDA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GRACE, ANTHONY A · 2003 to 2010
$2.4M
Stress-Induced Alterations in Amygdala-LC InteractionsR56DA015408 · NIDA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GRACE, ANTHONY A · 2012 to 2012
$74k
NIDA NIH HHS DA15408NIDA NIH HHS R01 DA015408NIDA NIH HHS R56 DA015408
6 · The paper itself

Abstract

Substantial data exists demonstrating the importance of the amygdala and the locus ceruleus (LC) in responding to stress, aversive memory formation, and the development of stress-related disorders; however, little is known about the effects of norepinephrine (NE) on amygdala neuronal activity in vivo. The basolateral nucleus of the amygdala (BLA) receives dense NE projections from the LC, NE increases in the BLA in response to stress, and the BLA can also modulate the LC via reciprocal projections. These experiments examined the effects of noradrenergic agents on spontaneous and evoked responses of BLA neurons. NE iontophoresis inhibited spontaneous firing and decreased the responsiveness of BLA neurons to electrical stimulation of entorhinal cortex and sensory association cortex (Te3). Confirmed BLA projection neurons exhibited exclusively inhibitory responses to NE. Systemic administration of propranolol, a beta-receptor antagonist, decreased the spontaneous firing rate and potentiated the NE-evoked inhibition of BLA neurons. In addition, iontophoresis of the alpha-2 agonist clonidine, footshock administration, and LC stimulation mimicked the effects of NE iontophoresis on spontaneous activity. Furthermore, the effects of LC stimulation were partially blocked by systemic administration of alpha 2 and beta receptor antagonists. This is the first study to demonstrate the actions of directly applied and stimulus-evoked NE in the BLA in vivo, and provides a mechanism by which beta receptors can mediate the important behavioral consequences of NE within the BLA. The interaction between these two structures is particularly relevant with regard to their known involvement in stress responses and stress-related disorders.

Indexed as

Action PotentialsAdrenergic alpha-2 Receptor AgonistsAmygdalaAnimalsMaleNeural InhibitionNeuronsNorepinephrineRatsRats, Sprague-DawleyReceptors, Adrenergic, alpha-2Receptors, Adrenergic, betaAdrenergic alpha-2 Receptor AgonistsNorepinephrineReceptors, Adrenergic, alpha-2Receptors, Adrenergic, beta

Identifiers

PMID17989300
PMCPMC6673273
OpenAlexW2014543037

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.