Evidence map›Paper›PMID 28328571›Full record

ArticlePain2017

Neuropathic pain-induced enhancement of spontaneous and pain-evoked neuronal activity in the periaqueductal gray that is attenuated by gabapentin.

Vijay K Samineni, Louis S Premkumar, Carl L Faingold

Abstract read
In one paragraph

Article in Pain, 2017. 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
2.5field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
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  12. Principles of nociceptive coding in the anterior cingulate cortex.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  13. Article
  14. Review
  15. Review
  16. Ventrolateral Periaqueductal Gray Astrocytes Regulate Nociceptive Sensation and Emotional Motivation in Diabetic Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  17. Review
  18. Review
  19. Neurotropin alleviates rat osteocarcinoma pain via PIranian journal of basic medical sciences · 2021
    Article
  20. 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

3 authors at 1 institution in 1 country.

Vijay K SamineniDepartment of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Louis S Premkumar
Carl L Faingold
Southern Illinois University School of Medicine · US

Funding

A Novel Approach for Chronic Pain Treatment Using ResiniferatoxinR01DA028017 · NIDA · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI PREMKUMAR, LOUIS S · 2009 to 2013
$1.4M
Endogenous Activators of Vanilloid ReceptorR01NS042296 · NINDS · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI PREMKUMAR, LOUIS S · 2001 to 2004
$782k
Vanilloid Receptors in Diabetic Peripheral NeuropathyR01DK065742 · NIDDK · SOUTHERN ILLINOIS UNIVERSITY SCH OF MED · PI PREMKUMAR, LOUIS S · 2004 to 2006
$766k
NIDA NIH HHS R01 DA028017NIDDK NIH HHS R01 DK065742NINDS NIH HHS R01 NS042296
6 · The paper itself

Abstract

Neuropathic pain is a debilitating pathological condition that is poorly understood. Recent evidence suggests that abnormal central processing occurs during the development of neuropathic pain induced by the cancer chemotherapeutic agent, paclitaxel. Yet, it is unclear what role neurons in supraspinal pain network sites, such as the periaqueductal gray, play in altered behavioral sensitivity seen during chronic pain conditions. To elucidate these mechanisms, we studied the spontaneous and thermally evoked firing patterns of ventrolateral periaqueductal gray (vlPAG) neurons in awake-behaving rats treated with paclitaxel to induce neuropathic pain. In the present study, vlPAG neurons in naive rats exhibited either excitatory, inhibitory, or neutral responses to noxious thermal stimuli, as previously observed. However, after development of behavioral hypersensitivity induced by the chemotherapeutic agent, paclitaxel, vlPAG neurons displayed increased neuronal activity and changes in thermal pain-evoked neuronal activity. This involved elevated levels of spontaneous firing and heightened responsiveness to nonnoxious stimuli (allodynia) as well as noxious thermal stimuli (hyperalgesia) as compared with controls. Furthermore, after paclitaxel treatment, only excitatory neuronal responses were observed for both nonnoxious and noxious thermal stimuli. Systemic administration of gabapentin, a nonopioid analgesic, induced significant dose-dependent decreases in the elevated spontaneous and thermally evoked vlPAG neuronal firing to both nonnoxious and noxious thermal stimuli in rats exhibiting neuropathic pain, but not in naive rats. Thus, these results show a strong correlation between behavioral hypersensitivity to thermal stimuli and increased firing of vlPAG neurons in allodynia and hyperalgesia that occur in this neuropathic pain model.

Indexed as

Action PotentialsAminesAnalgesicsAnimalsCyclohexanecarboxylic AcidsGabapentingamma-Aminobutyric AcidHot TemperatureMaleNeuralgiaNeuronal PlasticityNeuronsPaclitaxelPeriaqueductal GrayRatsRats, Sprague-DawleyAminesAnalgesicsCyclohexanecarboxylic AcidsGabapentingamma-Aminobutyric AcidPaclitaxel

Identifiers

PMID28328571
PMCPMC5474198
OpenAlexW2598459170

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.