ArticleBehavioural brain research2019
Reversal of ultrasonic vocalization deficits in a mouse model of Fragile X Syndrome with minocycline treatment or genetic reduction of MMP-9.
Article in Behavioural brain research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Brief Report: A Double-Blind, Placebo-Controlled, Crossover, Proof-of-Concept Study of Minocycline in Autism Spectrum Disorder.Journal of autism and developmental disorders · 2025Trial
- Article
- State-of-the-art therapies for fragile X syndrome.Developmental medicine and child neurology · 2024Review
- Sex-specific modulation of early life vocalization and cognition by Fmr1 gene dosage in a mouse model of Fragile X Syndrome.Biology of sex differences · 2024Article
- Long COVID elevated MMP-9 and release from microglia by SARS-CoV-2 Spike protein.Translational neuroscience · 2024Article
- Article
- Systemic immune profile in Prader-Willi syndrome: elevated matrix metalloproteinase and myeloperoxidase and reduced macrophage inhibitory factor.Orphanet journal of rare diseases · 2023Article
- Influence of Gestational Chlorpyrifos Exposure on ASD-like Behaviors in an fmr1-KO Rat Model.Molecular neurobiology · 2022Article
- Deletion of Fmr1 in parvalbumin-expressing neurons results in dysregulated translation and selective behavioral deficits associated with fragile X syndrome.Molecular autism · 2022Article
- Targeted therapy of cognitive deficits in fragile X syndrome.Molecular psychiatry · 2022Article
- Fragile X Syndrome: From Molecular Aspect to Clinical Treatment.International journal of molecular sciences · 2022Review
- EEG as a translational biomarker and outcome measure in fragile X syndrome.Translational psychiatry · 2022Review
- Neural Correlates of Auditory Hypersensitivity in Fragile X Syndrome.Frontiers in psychiatry · 2021Review
- Acute pharmacological inhibition of matrix metalloproteinase-9 activity during development restores perineuronal net formation and normalizes auditory processing in Fmr1 KO mice.Journal of neurochemistry · 2020Article
- Minocycline Treatment Reverses Sound Evoked EEG Abnormalities in a Mouse Model of Fragile X Syndrome.Frontiers in neuroscience · 2020Article
- A neurophysiological model of speech production deficits in fragile X syndrome.Brain communications · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Fragile X Syndrome (FXS) is a leading genetic cause of autism and intellectual disabilities. The Fmr1 knockout (KO) mouse is a commonly studied pre-clinical model of FXS. Adult male Fmr1 KO mice produce fewer ultrasonic vocalizations (USVs) during mating, suggestive of abnormal social communication. Minocycline treatment for 2 months from birth alleviates a number of FXS phenotypes in mice, including USV call rate deficits. In the current study, we investigated if treatment initiated past the early developmental period would be effective, given that in many cases, individuals with FXS are treated during later developmental periods. Wildtype (WT) and Fmr1 KO mice were treated with minocycline between postnatal day (P) 30 and P58. Mating-related USVs were then recorded from these mice between P75 and P90 and analyzed for call rate, duration, bandwidth, and peak frequency. Untreated Fmr1 KO mice call at a significantly reduced rate compared to untreated WT mice. After minocycline treatment from 1 to 2 months of age, WT and Fmr1 KO mice exhibited similar call rates, due to an increase in calling in the latter group. Minocycline is thought to be effective in reducing FXS symptoms by lowering matrix-metalloproteinase-9 (MMP-9) levels. To determine whether abnormal MMP-9 levels underlie USV deficits, we characterized USVs in Fmr1 KO mice which were heterozygous for MMP-9 (MMP-9
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