Evidence map›Paper›PMID 39975365›Full record

ArticlebioRxiv : the preprint server for biology2025

A cell type-specific mechanism driving the rapid antidepressant effects of transcranial magnetic stimulation.

Michael W Gongwer, Alex Qi, Alexander S Enos, Sophia A Rueda, Cassandra B Klune, Meelan Shari, Adrienne Q Kashay, Owen H Williams, Aliza Hacking, Jack P Riley and 6 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Michael W GongwerDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.ORCID 0000-0002-4506-1224
Alex QiSemel Institute for Neuroscience and Human Behavior, Department of Psychiatry, Neuromodulation Division, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Alexander S EnosDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Sophia A RuedaDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Cassandra B KluneDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Meelan ShariDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Adrienne Q KashaySemel Institute for Neuroscience and Human Behavior, Department of Psychiatry, Neuromodulation Division, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Owen H WilliamsDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Aliza HackingDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Jack P RileyDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Gary A WilkeDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Yihong YangNeuroimaging Research Branch, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA.
Hanbing LuNeuroimaging Research Branch, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA.
Andrew F LeuchterSemel Institute for Neuroscience and Human Behavior, Department of Psychiatry, Neuromodulation Division, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.
Laura A DeNardoDepartment of Physiology, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.ORCID 0000-0002-7607-4773
Scott A WilkeSemel Institute for Neuroscience and Human Behavior, Department of Psychiatry, Neuromodulation Division, David Geffen School of Medicine, University of California, Los Angeles; Los Angeles, CA 90095, USA.ORCID 0000-0002-7421-4015

Funding

UCLA-Caltech Medical Scientist Training ProgramT32GM008042 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A, DAWSON, DAVID WAYNE · 1985 to 2023
$29.9M
Training Grant in Neurobehavioral GeneticsT32NS048004 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEARDEN, CARRIE E, OPHOFF, ROEL A · 2004 to 2025
$5.8M
Role of prefrontal dopamine circuits in threat avoidance learningR01MH137461 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Laura Anne DeNardo, Scott Allen Wilke · 2024 to 2026
$2.2M
Role of prefrontostriatal circuits in effort-based, cost-benefit decision makingR01MH131858 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Scott Allen Wilke · 2023 to 2026
$2.1M
Prefrontal circuit mechanisms of repetitive transcranial magnetic stimulationR21MH133212 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WILKE, SCOTT ALLEN · 2023 to 2024
$429k
Investigating circuit-specific effects of high-frequency repetitive transcranial magnetic stimulationF30MH134633 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GONGWER, MICHAEL W. · 2023 to 2024
$81k
NIGMS NIH HHS T32 GM008042NIMH NIH HHS F30 MH134633NIMH NIH HHS R01 MH131858NIMH NIH HHS R01 MH137461NIMH NIH HHS R21 MH133212NINDS NIH HHS T32 NS048004
6 · The paper itself

Abstract

Repetitive transcranial magnetic stimulation (rTMS) is an emerging treatment for brain disorders, but its therapeutic mechanism is unknown. We developed a novel mouse model of rTMS with superior clinical face validity and investigated the neural mechanism by which accelerated intermittent theta burst stimulation (aiTBS) - the first rapid-acting rTMS antidepressant protocol - reversed chronic stress-induced behavioral deficits. Using fiber photometry, we showed that aiTBS drives distinct patterns of neural activity in intratelencephalic (IT) and pyramidal tract (PT) projecting neurons in dorsomedial prefrontal cortex (dmPFC). However, only IT neurons exhibited persistently increased activity during both aiTBS and subsequent depression-related behaviors. Similarly, aiTBS reversed stress-related loss of dendritic spines on IT, but not PT neurons, further demonstrating cell type-specific effects of stimulation. Finally, chemogenetic inhibition of dmPFC IT neurons during rTMS blocked the antidepressant-like behavioral effects of aiTBS. Thus, we demonstrate a prefrontal mechanism linking rapid aiTBS-driven therapeutic effects to cell type-specific circuit plasticity.

Identifiers

PMID39975365
PMCPMC11838264

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.