ArticleMolecular medicine reports2022
The GABAB receptor agonist STX209 reverses the autism‑like behaviour in an animal model of autism induced by prenatal exposure to valproic acid.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Valproate Exposure as anCNS & neurological disorders drug targets · 2025Pooled it
- Drug Repurposing for Treating NCOR-Related Intellectual Disability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Developmental Disturbances in Animal Models of Autism Spectrum Disorder.Developmental neurobiology · 2025Review
- GABAMedComm · 2025Review
- The Microbiome-Genetics Axis in Autism Spectrum Disorders: A Probiotic Perspective.International journal of molecular sciences · 2024Review
- Ethanolamine and Vinyl-Ether Moieties in Brain Phospholipids Modulate Behavior in Rats.NeuroSci · 2024Article
- Perindopril Ameliorates Sodium Valproate-Induced Rat Model of Autism: Involvement of Sirtuin-1, JAK2/STAT3 Axis, PI3K/Akt/GSK-3β Pathway, and PPAR-Gamma Signaling.Medicina (Kaunas, Lithuania) · 2024Article
- Solitary and Synergistic Effects of Different Hydrophilic and Hydrophobic Phospholipid Moieties on Rat Behaviors.Pharmaceutics · 2024Article
- Pre-autism: What a paediatrician should know about early diagnosis of autism.World journal of clinical pediatrics · 2023Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is a lifelong neurodevelopmental condition characterized by impaired social interaction, compromised communication, and restrictive or stereotyped behaviours and interests. Due to the complex pathophysiology of ASD, there are currently no available medical therapies for improving the associated social deficits. Consequently, the present study investigated the effects of STX209, a selective γ‑aminobutyric acid type B receptor (GABABR2) agonist, on an environmental rodent model of autism. The mouse model of autism induced by prenatal exposure to valproic acid (VPA) was used to assess the therapeutic potential of STX209 on autism‑like behaviour in the present study. This study investigated the effects of STX209 on VPA model mice via behavioral testing and revealed a significant reversal of core/associated autism‑like behavior, including sociability and preference for social novelty, novelty recognition, locomotion and exploration activity and marble‑burying deficit. This may be associated with STX209 correcting dendritic arborization, spine density and GABABR2 expression in hippocampus of VPA model mice. However, expression of glutamic acid decarboxylase 65/67 in the hippocampus were not altered by STX209. The present results demonstrated that STX209 administration ameliorated autism‑like symptoms in mice exposed to VPA prenatally, suggesting that autism‑like symptoms in children with a history of prenatal VPA exposure may also benefit from treatment with the GABABR2 agonist STX209.
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Registered trials
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.