Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing 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.
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
14 authors.
Emily G PeckDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.ORCID 0000-0002-2024-8930
Soren D EmersonDepartment of Pharmacology, Vanderbilt University, Nashville, TN 37232.
Alyson M CurryDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.ORCID 0000-0003-2996-4519
Kimberly M HolterDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.
Paige M EstaveDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.
Jonathon P SensDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.
Olivia A ColarussoDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.ORCID 0000-0003-0330-3894
Sean P FarrisDepartment of Anesthesiology, University of Pittsburgh, Pittsburgh, PA 15261.
Drew D KiralyDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.ORCID 0000-0002-4818-5169
Robert W GouldDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.ORCID 0000-0003-4861-1874
Brian A McCoolDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.ORCID 0000-0002-1002-9435
Erin S CalipariDepartment of Pharmacology, Vanderbilt University, Nashville, TN 37232.ORCID 0000-0003-4723-0623
Katherine M HolleranDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.ORCID 0000-0002-2931-8157
Sara R JonesDepartment of Translational Neuroscience, Wake Forest University School of Medicine, Winston-Salem, NC 27157.ORCID 0000-0002-3424-7576
Funding
TROPANE EVALUATION AND GENERAL SCIENTIFIC SERVICES COREP50DA006634 · NIDA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI HOWLETT, ALLYN C · 1991 to 2019
$30.8M
Wake Forest Translational Alcohol Research Center (WF-TARC)P50AA026117 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Paul W. Czoty · 2018 to 2026
$16.2M
MULTI-DISCIPLINARY TRAINING IN THE BIOLOGY OF ALCOHOLISMT32AA007565 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BRIAN A MCCOOL · 1994 to 2026
$10.1M
Role of noncoding RNA in alcohol actionU01AA020889 · NIAAA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Sean P Farris, Gregg E. Homanics · 2011 to 2026
$7.1M
The Ethanol - Anxiety Interaction: Cellular MechanismsR01AA014445 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCOOL, BRIAN A · 2004 to 2023
$5.2M
A Novel Animal Model of Cocaine AddictionR01DA014030 · NIDA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI JONES, SARA RAULERSON · 2001 to 2015
$3.2M
Kappa Opioid Receptors and Phospho-Dopamine Transporters Drive Cocaine RewardR01DA054694 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI LANKUPALLE D JAYANTHI, SARA RAULERSON JONES · 2022 to 2026
$3.2M
LNCRNA REGULATION OF GENE EXPRESSION & BEHAVIORR01AA030257 · NIAAA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Sean P Farris · 2022 to 2026
$2.8M
Mechanisms of dopaminergic dysfunction in substance use disorderR01DA052317 · NIDA · VANDERBILT UNIVERSITY · PI CALIPARI, ERIN · 2021 to 2025
$2.4M
Molecular determinants of ensemble recruitment by drugs of abuseR01DA062024 · NIDA · VANDERBILT UNIVERSITY · PI Erin Calipari · 2025 to 2026
$2.3M
The Neurobiology of Drug AbuseT32DA041349 · NIDA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI SARA RAULERSON JONES · 2017 to 2026
$1.8M
Dopamine Transporter Changes Following Cocaine Self-AdministrationR01DA021325 · NIDA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI JONES, SARA RAULERSON · 2007 to 2011
Cocaine use disorder is marked by deficits in dopamine signaling; however, the molecular mechanisms driving these deficits remain unclear. The synaptic vesicle protein Synaptogyrin-3 (Syngr3) has recently garnered attention for its association with disorders involving dopamine dysfunction and impaired cognition. Here, we found low Syngr3 expression in the ventral tegmental area (VTA) of men who died of cocaine overdose and in male rats that had chronically self-administered cocaine. Syngr3 was confirmed to be in dopamine neurons, and its expression was correlated with dopamine markers in both humans and rats. Syngr3 levels showed a robust inverse correlation with motivation to self-administer cocaine in the rat model. Moreover, viral overexpression of Syngr3 in VTA dopamine neurons improved cognitive flexibility and substantially reduced cocaine reinforcement and drug-taking behavior. Finally, Syngr3 overexpression prevented cocaine-induced dopamine deficits. These findings establish Syngr3 as a key dopamine regulator and potential therapeutic target for cocaine use disorder.
Indexed as
Cocaine-Related DisordersDopamineSynaptogyrinsAnimalsCocaineDopaminergic NeuronsHumansMaleRatsRats, Sprague-DawleyVentral Tegmental AreaCocaineDopamineSynaptogyrinscocaine use disorderdopaminedopamine transporterSynaptogyrin-3
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.
Synaptogyrin-3 plays a critical role in addiction-related dopamine dysfunction and behavioral maladaptations. · full record | OpenQuestion