Evidence map›Paper›PMID 26881134›Full record

ReviewNeural plasticity2016

Emerging Roles of BAI Adhesion-GPCRs in Synapse Development and Plasticity.

Joseph G Duman, Yen-Kuei Tu, Kimberley F Tolias

Abstract readReview
In one paragraph

Review in Neural plasticity, 2016. 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
–field-weighted citation impact
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.

  1. Article
  2. Adhesion G protein-coupled receptors.Pharmacological reviews · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Synaptic Gα12/13 signaling establishes hippocampal PV inhibitory circuits.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Review
  14. A Functional Schizophrenia-associated genetic variant near thebioRxiv : the preprint server for biology · 2023
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  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

3 authors.

Joseph G DumanDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Yen-Kuei TuDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Integrative Molecular and Biomedical Sciences Program, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Kimberley F ToliasDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Integrative Molecular and Biomedical Sciences Program, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

Funding

Signaling Mechanisms Regulating Rho GTPase-Dependent Synaptic Plasticity Underlying Memory in Health and DiseaseR01NS062829 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI TOLIAS, KIMBERLY R · 2009 to 2025
$4.4M
A MOLECULAR CODE FOR CONNECTIVITY IN THE NEOCORTEXR01MH103108 · NIMH · BAYLOR COLLEGE OF MEDICINE · PI TOLIAS, ANDREAS, TOLIAS, KIMBERLY R · 2013 to 2016
$1.3M
NIMH NIH HHS K01MH089112NIMH NIH HHS R01 MH103108NIMH NIH HHS R01MH103108NINDS NIH HHS R01 NS062829NINDS NIH HHS R01NS062829
6 · The paper itself

Abstract

Synapses mediate communication between neurons and enable the brain to change in response to experience, which is essential for learning and memory. The sites of most excitatory synapses in the brain, dendritic spines, undergo rapid remodeling that is important for neural circuit formation and synaptic plasticity. Abnormalities in synapse and spine formation and plasticity are associated with a broad range of brain disorders, including intellectual disabilities, autism spectrum disorders (ASD), and schizophrenia. Thus, elucidating the mechanisms that regulate these neuronal processes is critical for understanding brain function and disease. The brain-specific angiogenesis inhibitor (BAI) subfamily of adhesion G-protein-coupled receptors (adhesion-GPCRs) has recently emerged as central regulators of synapse development and plasticity. In this review, we will summarize the current knowledge regarding the roles of BAIs at synapses, highlighting their regulation, downstream signaling, and physiological functions, while noting the roles of other adhesion-GPCRs at synapses. We will also discuss the relevance of BAIs in various neurological and psychiatric disorders and consider their potential importance as pharmacological targets in the treatment of these diseases.

Indexed as

Neuronal PlasticityAngiogenic ProteinsAnimalsBrainDendritic SpinesHumansMental DisordersNerve Tissue ProteinsNervous System DiseasesReceptors, G-Protein-CoupledSignal TransductionSynapsesADGRB1 protein, humanADGRB2 protein, humanADGRB3 protein, humanAngiogenic ProteinsNerve Tissue ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID26881134
PMCPMC4736325

What OpenQuestion holds

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LicenceCC BY
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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.