Small molecule ion channel agonist/antagonist screen reveals seizure suppression via glial Irk2 activation in a Drosophila model of Dup15q syndrome.

Benjamin Geier, Bidisha Roy, Lawrence T Reiter

Abstract read

In one paragraph

Article in Neurobiology of disease, 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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

A dual-reporter mouse for therapeutic discovery in Angelman syndrome.JCI insight · 2026
Article

4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Benjamin GeierDepartment of Physiology, Tulane University, New Orleans, LA, USA; Graduate Program in Neuroscience, Tulane University, New Orleans, LA, USA.

Bidisha RoyDepartment of Neurology, University of Tennessee Health Science Center, Memphis, TN, USA.

Lawrence T ReiterDepartment of Physiology, Tulane University, New Orleans, LA, USA. Electronic address: lreiter@tulane.edu.

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026

$13.5M

The role of UBE3A in gliopathic seizuresR01NS115776 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI REITER, LAWRENCE T, ZAKHARENKO, STANISLAV S · 2020 to 2024

$2.0M

NIH HHS P40 OD018537NINDS NIH HHS R01 NS115776

6 · The paper itself

Abstract

The neurogenetic disorder duplication 15q syndrome (Dup15q) is characterized by a high incidence of autism spectrum disorder (ASD) and pharmacoresistant epilepsy. Standard-of-care broad-spectrum anti-seizure medications (ASM) often fail to control seizures in Dup15q, emphasizing the need for the identification of new therapeutic compounds. Previously, we generated a model of Dup15q in Drosophila melanogaster by overexpressing Dube3a in glial cells, instead of neurons. This model recapitulates the spontaneous seizures present in Dup15q patients. Here, we screened a set of FDA-approved compounds for their ability to suppress seizures in repo > Dube3a flies. We used 72 compounds from the Enzo SCREEN-WELL Ion Channel Library for primary screening of seizure suppression. Six compounds were identified that significantly reduced seizure duration. Furthermore, the compounds that passed the primary and secondary screenings were associated with K

Indexed as

AnticonvulsantsDrosophila ProteinsNeurogliaPotassium Channels, Inwardly RectifyingSeizuresAnimalsAnimals, Genetically ModifiedDisease Models, AnimalDrosophila melanogasterAnticonvulsantsDrosophila ProteinsPotassium Channels, Inwardly RectifyingDrosophilaDrug screenDup15q syndromeEpilepsyIon channels

Identifiers

PMID40122181

DOI10.1016/j.nbd.2025.106882

PMCPMC12117380

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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.