Evidence map›Paper›PMID 15574363›Full record

ReviewFrontiers in bioscience : a journal and virtual library2005

Pathobiology of dynorphins in trauma and disease.

Kurt F Hauser, Jane V Aldrich, Kevin J Anderson, Georgy Bakalkin, MacDonald J Christie, Edward D Hall, Pamela E Knapp, Stephen W Scheff, Indrapal N Singh, Bryce Vissel and 3 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Frontiers in bioscience : a journal and virtual library, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

50 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
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  13. Article
  14. Mechanism and site of action of big dynorphin on ASIC1a.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Article
  16. Article
  17. Intra- and interregional coregulation of opioid genes: broken symmetry in spinal circuits.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  18. Review
  19. Article
  20. Review
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

13 authors at 1 institution in 1 country.

Kurt F HauserDepartment of Anatomy and Neurobiology, University of Kentucky College of Medicine, Lexington, Kentucky 40536-0298, USA. khauser@uky.edu
Jane V Aldrich
Kevin J Anderson
Georgy Bakalkin
MacDonald J Christie
Edward D Hall
Pamela E Knapp
Stephen W Scheff
Indrapal N Singh
Bryce Vissel
Amina S Woods
Tatiana Yakovleva
Toni S Shippenberg
University of Kentucky · US

Funding

OPIOIDS AND CENTRAL NERVOUS SYSTEM VULNERABILITY TO HIVR01DA013559 · NIDA · UNIVERSITY OF KENTUCKY · PI HAUSER, KURT F · 2000 to 2004
$1.4M
Modulation of Repeated Ethanol AdministrationU01AA013486 · NIAAA · UNIVERSITY OF TEXAS AUSTIN · PI GONZALES, RUEBEN A · 2001 to 2005
$1.2M
Opioids Modulate Oligodendrocyte Development &FunctionR01DA015097 · NIDA · UNIVERSITY OF KENTUCKY · PI KNAPP, PAMELA E · 2003 to 2006
$1.0M
NEUROCHEMICAL INTERACTIONS AND BEHAVIOR SEQUELLA IN MODELS OF DRUG ABUSEZ01DA000398 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI SHIPPENBERG, TONI S. · 1997 to 2006
–
NIAAA NIH HHS AA13486-03NIAAA NIH HHS U01 AA013486NIDA NIH HHS DA13359NIDA NIH HHS DA15097NIDA NIH HHS R01 DA013559NIDA NIH HHS R01 DA015097
6 · The paper itself

Abstract

Dynorphins, endogenous opioid neuropeptides derived from the prodynorphin gene, are involved in a variety of normative physiologic functions including antinociception and neuroendocrine signaling, and may be protective to neurons and oligodendroglia via their opioid receptor-mediated effects. However, under experimental or pathophysiological conditions in which dynorphin levels are substantially elevated, these peptides are excitotoxic largely through actions at glutamate receptors. Because the excitotoxic actions of dynorphins require supraphysiological concentrations or prolonged tissue exposure, there has likely been little evolutionary pressure to ameliorate the maladaptive, non-opioid receptor mediated consequences of dynorphins. Thus, dynorphins can have protective and/or proapoptotic actions in neurons and glia, and the net effect may depend upon the distribution of receptors in a particular region and the amount of dynorphin released. Increased prodynorphin gene expression is observed in several disease states and disruptions in dynorphin processing can accompany pathophysiological situations. Aberrant processing may contribute to the net negative effects of dysregulated dynorphin production by tilting the balance towards dynorphin derivatives that are toxic to neurons and/or oligodendroglia. Evidence outlined in this review suggests that a variety of CNS pathologies alter dynorphin biogenesis. Such alterations are likely maladaptive and contribute to secondary injury and the pathogenesis of disease.

Indexed as

Gene Expression RegulationAnimalsApoptosisDynorphinsEvolution, MolecularHumansNeurogliaNeuronsNeuropeptidesReceptors, OpioidSpinal Cord InjuriesDynorphinsNeuropeptidesReceptors, Opioid

Identifiers

PMID15574363
PMCPMC4304872
OpenAlexW187333225

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.