Evidence map›Paper›PMID 25846623›Full record

ReviewHandbook of experimental pharmacology2015

Amygdala pain mechanisms.

Volker Neugebauer

Open access · greenAbstract readReview
In one paragraph

Review in Handbook of experimental pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 241 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
241citing papers in PubMed, 3 pooled it
144.2field-weighted citation impact, top 1% 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

241 citing papers in PubMed, 3 syntheses or guidelines pooled it, 386 citations in OpenAlex.

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  11. Central amygdalar PKCδ neurons mediate fentanyl withdrawal.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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181 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

1 author at 1 institution in 1 country.

Volker NeugebauerDepartment of Pharmacology and Neuroscience, Center for Translational Neuroscience and Therapeutics, Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX, 79430-6592, USA, volker.neugebauer@ttuhsc.edu.
Texas Tech University Health Sciences Center · US

Funding

VISCERAL PAINP01NS011255 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI CHUNG, JIN M · 1985 to 2012
$13.6M
PAIN, NOCICEPTION, AND THE AMYGDALAR01NS038261 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI Volker Neugebauer, Igor Ponomarev · 1999 to 2026
$8.7M
Amygdala Serotonin Neurotransmission and Neuropathic PainR01NS081121 · NINDS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GREEN, THOMAS ARTHUR, NEUGEBAUER, VOLKER · 2013 to 2017
$2.3M
NINDS NIH HHS NS-081121NINDS NIH HHS NS-11255NINDS NIH HHS NS-38261NINDS NIH HHS P01 NS011255NINDS NIH HHS R01 NS038261NINDS NIH HHS R01 NS081121
6 · The paper itself

Abstract

A limbic brain area, the amygdala plays a key role in emotional responses and affective states and disorders such as learned fear, anxiety, and depression. The amygdala has also emerged as an important brain center for the emotional-affective dimension of pain and for pain modulation. Hyperactivity in the laterocapsular division of the central nucleus of the amygdala (CeLC, also termed the "nociceptive amygdala") accounts for pain-related emotional responses and anxiety-like behavior. Abnormally enhanced output from the CeLC is the consequence of an imbalance between excitatory and inhibitory mechanisms. Impaired inhibitory control mediated by a cluster of GABAergic interneurons in the intercalated cell masses (ITC) allows the development of glutamate- and neuropeptide-driven synaptic plasticity of excitatory inputs from the brainstem (parabrachial area) and from the lateral-basolateral amygdala network (LA-BLA, site of integration of polymodal sensory information). BLA hyperactivity also generates abnormally enhanced feedforward inhibition of principal cells in the medial prefrontal cortex (mPFC), a limbic cortical area that is strongly interconnected with the amygdala. Pain-related mPFC deactivation results in cognitive deficits and failure to engage cortically driven ITC-mediated inhibitory control of amygdala processing. Impaired cortical control allows the uncontrolled persistence of amygdala pain mechanisms.

Indexed as

AmygdalaAnimalsCalcitoninCorticotropin-Releasing Hormonegamma-Aminobutyric AcidHumansNeuronal PlasticityNeuropeptidesPainProtein PrecursorsReceptor, Metabotropic Glutamate 5Receptors, N-Methyl-D-AspartateCalcitoninCorticotropin-Releasing Hormonegamma-Aminobutyric AcidNeuropeptidesneuropeptide S, humanProtein PrecursorsReceptor, Metabotropic Glutamate 5Receptors, N-Methyl-D-Aspartate

Identifiers

PMID25846623
PMCPMC4701385
OpenAlexW2409837131

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.