Evidence map›Paper›PMID 24639635›Full record

ArticleFrontiers in behavioral neuroscience2014

Inhibition of PKC disrupts addiction-related memory.

Kristin K Howell, Bradley R Monk, Stephanie A Carmack, Oliver D Mrowczynski, Robert E Clark, Stephan G Anagnostaras

Open access · goldAbstract read
In one paragraph

Article in Frontiers in behavioral neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Reversing Cocaine-Induced Plasticity with Zeta Inhibitory Peptide.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. S-Glutathionylation and Redox Protein Signaling in Drug Addiction.Progress in molecular biology and translational science · 2016
    Article
  11. 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

6 authors at 1 institution in 1 country.

Kristin K HowellMolecular Cognition Laboratory, Department of Psychology, University of California San Diego, La Jolla, CA, USA.
Bradley R MonkMolecular Cognition Laboratory, Department of Psychology, University of California San Diego, La Jolla, CA, USA.
Stephanie A CarmackMolecular Cognition Laboratory, Department of Psychology, University of California San Diego, La Jolla, CA, USA.
Oliver D MrowczynskiDivision of Biological Sciences, University of California San Diego, La Jolla, CA, USA.
Robert E ClarkVeterans Affairs Medical Center San Diego, CA, USA ; Department of Psychiatry, University of California San Diego, La Jolla, CA, USA.
Stephan G AnagnostarasMolecular Cognition Laboratory, Department of Psychology, University of California San Diego, La Jolla, CA, USA ; Program in Neurosciences, University of California San Diego, La Jolla, CA, USA.
University of California, San Diego · US

Funding

Molecular Cognition of AddictionR01DA020041 · NIDA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ANAGNOSTARAS, STEPHAN G · 2007 to 2011
$1.5M
NIDA NIH HHS R01 DA020041
6 · The paper itself

Abstract

The atypical PKC isoforms, PKMζ and PKCλ have been proposed as integral substrates of long-term memory (LTM). Inhibition of these isoforms has recently been demonstrated to be sufficient for impairing the expression and maintenance of long-term potentiation. Additionally, the pseudosubstrate inhibitor, zeta inhibitory peptide (ZIP), which effectively blocks PKMζ and PKCλ, has previously been shown to disrupt associative memory; very little is known about its effects on pathological nonassociative forms of memory related to addiction. The neural and molecular substrates of memory and addiction have recently been argued to overlap. Here, we used ZIP to disrupt PKMζ and PKCλ activity to examine their role in cocaine sensitization, a nonassociative, addiction-related memory argued to underlie the transition from casual to pathological drug use. We examined the effects of both continuous and acute administration of ZIP. Even a single application of ZIP blocked the development of sensitization; sustained inhibition using osmotic pumps produced an almost complete blockade of sensitization. Further, a single application of ZIP was shown to reduce membrane-bound AMPAR expression. These results demonstrate a novel, critical role for the atypical PKC isoforms in nonassociative memory and cocaine addiction.

Indexed as

cocainememorynonassociativePKCsensitizationZIP

Identifiers

PMID24639635
PMCPMC3945752
OpenAlexW1976296068

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.