Evidence map›Paper›PMID 29258653›Full record

ReviewBiological psychiatry2018

Exploring the Role of Astroglial Glutamate Release and Association With Synapses in Neuronal Function and Behavior.

Michael D Scofield

Abstract readReviewVideo-Audio Media
In one paragraph

Review in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
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  4. Article
  5. "Unraveling the role ofReceptors (Basel, Switzerland) · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
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  12. Astrocyte regulation of synaptic signaling in psychiatric disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
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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

1 author at 1 institution in 1 country.

Michael D ScofieldDepartment of Anesthesiology and Perioperative Medicine, Medical University of South Carolina, Charleston, South Carolina; Department of Neuroscience, Medical University of South Carolina, Charleston, South Carolina. Electronic address: scofield@musc.edu.
Medical University of South Carolina · US

Funding

Contributions of Nitrergic Interneurons and NO Signaling in Cocaine RelapseR00DA040004 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SCOFIELD, MICHAEL DAVID · 2017 to 2019
$747k
Contributions of Nitrergic Interneurons and NO Signaling in Cocaine RelapseK99DA040004 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SCOFIELD, MICHAEL DAVID · 2015 to 2016
$297k
NIDA NIH HHS K99 DA040004NIDA NIH HHS R00 DA040004
6 · The paper itself

Abstract

Astrocytes are stellate cells whose appearance can resemble a pointed star, especially when visualizing glial fibrillary acidic protein, a canonical marker for astrocytes. Accordingly, there is a commonly made connection between the points of light that shine in the night sky and the diffuse and abundant cells that buffer ions and provide support for neurons. An exceptional amount of function has been attributed to, negated for, and potentially reaffirmed for these cells, especially regarding their ability to release neuroactive molecules and influence synaptic plasticity. This makes the precise role of astrocytes in tuning neural communication seem difficult to grasp. However, data from animal models of addiction demonstrate that a variety of drug-induced molecular adaptations responsible for relapse vulnerability take place in astrocyte systems that regulate glutamate uptake and release. These findings highlight astrocytes as a critical component of the neural systems responsible for addiction, serving as a key component of the plasticity responsible for relapse and drug seeking. Here I assemble recent findings that utilize genetic tools to selectively manipulate or measure flux of internal calcium in astrocytes, focusing on G protein-coupled receptor-mediated mobilization of calcium and the induction of glutamate release. Further, I compile evidence regarding astrocyte glutamate release as well as astrocyte association with synapses with respect to the impact of these cellular phenomena in shaping synaptic transmission. I also place these findings in the context of the previous studies of Scofield et al., who explored the role of astrocytes in the nucleus accumbens in the neural mechanisms underlying cocaine seeking.

Indexed as

AnimalsAstrocytesCalcium Channels, N-TypeCocaineDopamine Uptake InhibitorsDrug-Seeking BehaviorGlial Fibrillary Acidic ProteinGlutamic AcidHumansNeuronal PlasticityNeuronsNucleus AccumbensSynapsesSynaptic TransmissionCalcium Channels, N-TypeCocaineDopamine Uptake InhibitorsGlial Fibrillary Acidic ProteinGlutamic AcidAstrocyteCalciumCocaineGliotransmissionGlutamateGPCR

Identifiers

PMID29258653
PMCPMC5948108
OpenAlexW2767323726

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.