Evidence map›Paper›PMID 20144185›Full record

ArticleMolecular pain2010

Facilitation of synaptic transmission and pain responses by CGRP in the amygdala of normal rats.

Jeong S Han, Hita Adwanikar, Zhen Li, Guangchen Ji, Volker Neugebauer

Abstract read
In one paragraph

Article in Molecular pain, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing 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

84 citing papers in PubMed.

  1. Article
  2. Article
  3. Central amygdalar PKCδ neurons mediate fentanyl withdrawal.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Sex Differences in Central Amygdala Glutamate Responses to Calcitonin Gene-Related Peptide.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

24 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

5 authors.

Jeong S HanDepartment of Neuroscience & Cell Biology, The University of Texas Medical Branch, Galveston, Texas 77555-1069, USA.
Hita Adwanikar
Zhen Li
Guangchen Ji
Volker Neugebauer

Funding

VISCERAL PAINP01NS011255 · NINDS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI NEUGEBAUER, VOLKER · 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
NINDS NIH HHS NS-11255NINDS NIH HHS NS-38261NINDS NIH HHS R01 NS038261
6 · The paper itself

Abstract

Calcitonin gene-related peptide (CGRP) plays an important role in peripheral and central sensitization. CGRP also is a key molecule in the spino-parabrachial-amygdaloid pain pathway. Blockade of CGRP1 receptors in the spinal cord or in the amygdala has antinociceptive effects in different pain models. Here we studied the electrophysiological mechanisms of behavioral effects of CGRP in the amygdala in normal animals without tissue injury.Whole-cell patch-clamp recordings of neurons in the latero-capsular division of the central nucleus of the amygdala (CeLC) in rat brain slices showed that CGRP (100 nM) increased excitatory postsynaptic currents (EPSCs) at the parabrachio-amygdaloid (PB-CeLC) synapse, the exclusive source of CGRP in the amygdala. Consistent with a postsynaptic mechanism of action, CGRP increased amplitude, but not frequency, of miniature EPSCs and did not affect paired-pulse facilitation. CGRP also increased neuronal excitability. CGRP-induced synaptic facilitation was reversed by an NMDA receptor antagonist (AP5, 50 microM) or a PKA inhibitor (KT5720, 1 microM), but not by a PKC inhibitor (GF109203X, 1 microM). Stereotaxic administration of CGRP (10 microM, concentration in microdialysis probe) into the CeLC by microdialysis in awake rats increased audible and ultrasonic vocalizations and decreased hindlimb withdrawal thresholds. Behavioral effects of CGRP were largely blocked by KT5720 (100 microM) but not by GF109203X (100 microM).The results show that CGRP in the amygdala exacerbates nocifensive and affective behavioral responses in normal animals through PKA- and NMDA receptor-dependent postsynaptic facilitation. Thus, increased CGRP levels in the amygdala might trigger pain in the absence of tissue injury.

Indexed as

AmygdalaAnimalsCalcitonin Gene-Related PeptidePainRatsRats, Sprague-DawleySynaptic TransmissionCalcitonin Gene-Related Peptide

Identifiers

PMID20144185
PMCPMC2829526

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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.