Evidence map›Paper›PMID 23699055›Full record

ArticleJournal of neurophysiology2013

Fear signaling in the prelimbic-amygdala circuit: a computational modeling and recording study.

Sandeep Pendyam, Christian Bravo-Rivera, Anthony Burgos-Robles, Francisco Sotres-Bayon, Gregory J Quirk, Satish S Nair

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Emotional Memory Processing during REM Sleep with Implications for Post-Traumatic Stress Disorder.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  8. Review
  9. Article
  10. Hippocampal Inputs in the Prelimbic Cortex Curb Fear after Extinction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Metabotropic glutamate receptor 3 activation is required for long-term depression in medial prefrontal cortex and fear extinction.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
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

6 authors.

Sandeep PendyamDepartment of Electrical and Computer Engineering, University of Missouri, Columbia, Missouri 65211, USA.
Christian Bravo-Rivera
Anthony Burgos-Robles
Francisco Sotres-Bayon
Gregory J Quirk
Satish S Nair

Funding

Prefrontal-Amygdala Interactions in Fear ConditioningR01MH058883 · NIMH · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI BRAVO-RIVERA, CHRISTIAN EMMANUELL · 2003 to 2022
$4.3M
Translational Studies of Prefrontal Control of Fear ExtinctionR01MH081975 · NIMH · UNIVERSITY OF PUERTO RICO MED SCIENCES · PI QUIRK, GREGORY J · 2009 to 2013
$3.3M
CRCNS: Modeling Acquisition and Extinction of Fear Memories in Amygdala CircuitsR01MH087755 · NIMH · UNIVERSITY OF MISSOURI-COLUMBIA · PI NAIR, SATISH S · 2009 to 2011
$728k
NIMH NIH HHS R01 MH058883NIMH NIH HHS R01-MH058883NIMH NIH HHS R01 MH081975NIMH NIH HHS R01-MH081975NIMH NIH HHS R01 MH087755NIMH NIH HHS R01-MH087755
6 · The paper itself

Abstract

The acquisition and expression of conditioned fear depends on prefrontal-amygdala circuits. Auditory fear conditioning increases the tone responses of lateral amygdala neurons, but the increase is transient, lasting only a few hundred milliseconds after tone onset. It was recently reported that that the prelimbic (PL) prefrontal cortex transforms transient lateral amygdala input into a sustained PL output, which could drive fear responses via projections to the lateral division of basal amygdala (BL). To explore the possible mechanisms involved in this transformation, we developed a large-scale biophysical model of the BL-PL network, consisting of 850 conductance-based Hodgkin-Huxley-type cells, calcium-based learning, and neuromodulator effects. The model predicts that sustained firing in PL can be derived from BL-induced release of dopamine and norepinephrine that is maintained by PL-BL interconnections. These predictions were confirmed with physiological recordings from PL neurons during fear conditioning with the selective β-blocker propranolol and by inactivation of BL with muscimol. Our model suggests that PL has a higher bandwidth than BL, due to PL's decreased internal inhibition and lower spiking thresholds. It also suggests that variations in specific microcircuits in the PL-BL interconnection can have a significant impact on the expression of fear, possibly explaining individual variability in fear responses. The human homolog of PL could thus be an effective target for anxiety disorders.

Indexed as

Models, NeurologicalAcoustic StimulationAmygdalaAnimalsConditioning, PsychologicalFearMaleNeural PathwaysNeuronsPrefrontal CortexRatsRats, Sprague-Dawleyfear conditioningmuscimolneuromodulatortone response

Identifiers

PMID23699055
PMCPMC3742978

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.