Evidence map›Paper›PMID 28555077›Full record

ArticleMolecular psychiatry2018

The dendritic spine morphogenic effects of repeated cocaine use occur through the regulation of serum response factor signaling.

M E Cahill, D M Walker, A M Gancarz, Z J Wang, C K Lardner, R C Bagot, R L Neve, D M Dietz, E J Nestler

Abstract read
In one paragraph

Article in Molecular psychiatry, 2018. 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
2.1field-weighted citation impact, top 13% 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, 51 citations in OpenAlex.

  1. Review
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  3. Review
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  5. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
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  8. Review
  9. Review
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  11. A high-affinity cocaine binding site associated with the brain acid soluble protein 1.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cocaine Administration and Its Abstinence Conditions Modulate Neuroglia.International journal of molecular sciences · 2020
    Article
  18. Article
  19. 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

9 authors at 4 institutions in 2 countries.

M E CahillFishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
D M WalkerFishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
A M GancarzDepartment of Pharmacology and Toxicology, Research Institute on Addictions, Program in Neuroscience, State University at Buffalo, Buffalo, NY, USA.
Z J WangDepartment of Pharmacology and Toxicology, Research Institute on Addictions, Program in Neuroscience, State University at Buffalo, Buffalo, NY, USA.
C K LardnerFishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
R C BagotFishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
R L NeveDepartment of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
D M DietzDepartment of Pharmacology and Toxicology, Research Institute on Addictions, Program in Neuroscience, State University at Buffalo, Buffalo, NY, USA.
E J NestlerFishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Icahn School of Medicine at Mount Sinai · USUniversity at Buffalo, State University of New York · USAllen Institute for Brain Science · USInstitute of Cognitive and Brain Sciences · US

Funding

TRANSGENIC COREP01DA008227 · NIDA · YALE UNIVERSITY · PI NESTLER, ERIC J. · 1993 to 2018
$28.1M
Neurotrophic Mechanisms in Opiate and Cocaine ActionR01DA014133 · NIDA · UT SOUTHWESTERN MEDICAL CENTER · PI ERIC J. NESTLER · 2000 to 2026
$12.1M
MOLECULAR STUDIES OF COCAINE ACTION IN BRAINR37DA007359 · NIDA · YALE UNIVERSITY · PI NESTLER, ERIC J. · 1996 to 2020
$6.9M
Glial-mediated synaptic remodeling in drug addictionR01DA040620 · NIDA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Yan Dong, ERIC J. NESTLER · 2016 to 2026
$5.3M
Cocaine-induced neuroplasticity: a new role for TGF beta signalingR01DA037257 · NIDA · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI DIETZ, DAVID M · 2014 to 2018
$2.1M
NIDA NIH HHS P01 DA008227NIDA NIH HHS R01 DA014133NIDA NIH HHS R01 DA037257NIDA NIH HHS R01 DA040620NIDA NIH HHS R37 DA007359
6 · The paper itself

Abstract

The nucleus accumbens (NAc) is a primary brain reward region composed predominantly of medium spiny neurons (MSNs). In response to early withdrawal from repeated cocaine administration, de novo dendritic spine formation occurs in NAc MSNs. Much evidence indicates that this new spine formation facilitates the rewarding properties of cocaine. Early withdrawal from repeated cocaine also produces dramatic alterations in the transcriptome of NAc MSNs, but how such alterations influence cocaine's effects on dendritic spine formation remain unclear. Studies in non-neuronal cells indicate that actin cytoskeletal regulatory pathways in nuclei have a direct role in the regulation of gene transcription in part by controlling the access of co-activators to their transcription factor partners. In particular, actin state dictates the interaction between the serum response factor (SRF) transcription factor and one of its principal co-activators, MAL. Here we show that cocaine induces alterations in nuclear F-actin signaling pathways in the NAc with associated changes in the nuclear subcellular localization of SRF and MAL. Using in vivo optogenetics, the brain region-specific inputs to the NAc that mediate these nuclear changes are investigated. Finally, we demonstrate that regulated SRF expression, in turn, is critical for the effects of cocaine on dendritic spine formation and for cocaine-mediated behavioral sensitization. Collectively, these findings reveal a mechanism by which nuclear-based changes influence the structure of NAc MSNs in response to cocaine.

Indexed as

ActinsAnimalsCocaineCocaine-Related DisordersDendritesDendritic SpinesDopamine Uptake InhibitorsMaleMiceMice, Inbred C57BLMicroRNAsMyelin and Lymphocyte-Associated Proteolipid ProteinsNeurogenesisNeuronsNucleus AccumbensRewardActinsCocaineDopamine Uptake InhibitorsMal protein, mouseMicroRNAsMIRN132 microRNA, mouseMIRN212 microRNA, mouseMyelin and Lymphocyte-Associated Proteolipid ProteinsSerum Response Factor

Identifiers

PMID28555077
PMCPMC5709273
OpenAlexW2619236908

What OpenQuestion holds

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Registered trials

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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.