Evidence map›Paper›PMID 23433248›Full record

ReviewMolecular pain2013

ZIPping to pain relief: the role (or not) of PKMζ in chronic pain.

Theodore J Price, Sourav Ghosh

Open access · goldAbstract readReview
In one paragraph

Review in Molecular pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Spinal dopaminergic projections control the transition to pathological pain plasticity via a D1/D5-mediated mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  13. Article
  14. Article
  15. Review
  16. The pharmacology of nociceptor priming.Handbook of experimental pharmacology · 2015
    Review
  17. Article
  18. Cellular and subcellular localization of PKMζ.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Article
  19. Long-term potentiation in the anterior cingulate cortex and chronic pain.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
  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

2 authors at 1 institution in 1 country.

Theodore J PriceDepartment of Pharmacology, The University of Arizona School of Medicine, Arizona, USA. tjprice@email.arizona.edu
Sourav Ghosh
University of Arizona · US

Funding

Translation Control of Pain PlasticityR01NS065926 · NINDS · UNIVERSITY OF TEXAS DALLAS · PI PRICE, THEODORE J. · 2010 to 2023
$5.7M
Apical-basal polarity signaling in glioblastomaR01CA149258 · NCI · YALE UNIVERSITY · PI GHOSH, SOURAV · 2010 to 2014
$1.7M
NCI NIH HHS R01 CA149258NCI NIH HHS R01CA149258NINDS NIH HHS R01NS065926
6 · The paper itself

Abstract

Chronic pain remains a significant clinical problem despite substantial advances in our understanding of how persistent nociceptor stimulation drives plasticity in the CNS. A major theme that has emerged in this area of work is the strong similarity between plasticity involved in learning and memory in CNS regions such as cortex and hippocampus with mechanisms underlying chronic pain development and maintenance in the spinal dorsal horn and other CNS areas such as anterior cingulate cortex (ACC). We, and others have recently implicated an atypical PKC (aPKC), called PKMζ, in the maintenance of pain plasticity based on biochemical assays and the use of a peptide pseudosubstrate inhibitor called ZIP. These studies indicate remarkable parallels between the potential role of PKMζ as a key molecule for the maintenance of long-term memory and long-term potentiation (LTP) and the maintenance of a chronic pain state. On the other hand, very recent studies have disputed the specificity of ZIP and called into question the role of PKMζ as a memory maintenance molecule. Here we critically review the evidence that PKMζ might represent a new target for the reversal of certain chronic pain states. Furthermore, we consider whether ZIP might have other aPKC or even non-aPKC targets and the significance of such off-target effects for evaluating maintenance mechanisms of chronic pain. We conclude that, current controversies aside, utilization of ZIP as a tool to interrogate maintenance mechanisms of chronic pain and further investigations into the potential role of PKMζ, and other aPKCs, in pain plasticity are likely to lead to further insights with the potential to unravel the enigma that is the disease of chronic pain.

Indexed as

AnimalsCell-Penetrating PeptidesChronic PainEnzyme InhibitorsHumansLipopeptidesLong-Term PotentiationModels, BiologicalProtein Kinase CProtein Kinase C zetaCell-Penetrating PeptidesEnzyme InhibitorsLipopeptidesProtein Kinase CProtein Kinase C zetazeta-inhibitory peptide

Identifiers

PMID23433248
PMCPMC3621284
OpenAlexW2103987884

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.