Evidence map›Paper›PMID 39754065›Full record

ArticleJournal of neurodevelopmental disorders2025

Acute administration of NLX-101, a Serotonin 1A receptor agonist, improves auditory temporal processing during development in a mouse model of Fragile X Syndrome.

Xin Tao, Katilynne Croom, Adrian Newman-Tancredi, Mark Varney, Khaleel A Razak

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Article in Journal of neurodevelopmental disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
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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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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

3 citing papers in PubMed.

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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

5 authors.

Xin TaoGraduate Neuroscience Program, University of California, Riverside, CA, USA.
Katilynne CroomGraduate Neuroscience Program, University of California, Riverside, CA, USA.
Adrian Newman-TancrediNeurolixis SAS, Castres, France.
Mark VarneyNeurolixis SAS, Castres, France.
Khaleel A RazakGraduate Neuroscience Program, University of California, Riverside, CA, USA. khaleel@ucr.edu.

Funding

Eunice Kennedy Shriver National Institute of Child Health and Human Development 1U54HD104461-01
6 · The paper itself

Abstract

backgroundFragile X syndrome (FXS) is a leading known genetic cause of intellectual disability and autism spectrum disorders (ASD)-associated behaviors. A consistent and debilitating phenotype of FXS is auditory hypersensitivity that may lead to delayed language and high anxiety. Consistent with findings in FXS human studies, the mouse model of FXS, the Fmr1 knock out (KO) mouse, shows auditory hypersensitivity and temporal processing deficits. In electroencephalograph (EEG) recordings from humans and mice, these deficits manifest as increased N1 amplitudes in event-related potentials (ERP), increased gamma band single trial power (STP) and reduced phase locking to rapid temporal modulations of sound. In our previous study, we found that administration of the selective serotonin-1 A (5-HT

methodsTo test this hypothesis, we examined the effect of NLX-101 on EEG phenotypes in male and female wildtype (WT) and Fmr1 KO mice. Using epidural electrodes, we recorded auditory event related potentials (ERP) and auditory temporal processing with a gap-in-noise auditory steady state response (ASSR) paradigm at two ages, postnatal (P) 21 and 30 days, from both auditory and frontal cortices of awake, freely moving mice, following NLX-101 (at 1.8 mg/kg i.p.) or saline administration.

resultsSaline-injected Fmr1 KO mice showed increased N1 amplitudes, increased STP and reduced phase locking to auditory gap-in-noise stimuli versus wild-type mice, reproducing previously published EEG phenotypes. An acute injection of NLX-101 did not alter ERP amplitudes at either P21 or P30, but significantly reduces STP at P30. Inter-trial phase clustering was significantly increased in both age groups with NLX-101, indicating improved temporal processing. The differential effects of serotonin modulation on ERP, background power and temporal processing suggest different developmental mechanisms leading to these phenotypes.

conclusionsThese results suggest that NLX-101 could constitute a promising treatment option for targeting post-synaptic 5-HT

Indexed as

Disease Models, AnimalFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeMice, KnockoutAnimalsAuditory PerceptionElectroencephalographyEvoked Potentials, AuditoryFemaleMaleMiceMice, Inbred C57BLSerotonin 5-HT1 Receptor AgonistsFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1Serotonin 5-HT1 Receptor Agonists5-HT1A receptorsAutism spectrum disordersFragile X syndromeSensory hypersensitivitySerotoninSpeech processingTemporal processing

Identifiers

PMID39754065
PMCPMC11697955

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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.