Cited by 527Genetics and Neurodevelopmental DisordersNeuroscience and Neuropharmacology ResearchEpilepsy research and treatment

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Suppression of two major Fragile X Syndrome mouse model phenotypes by the mGluR5 antagonist MPEP

Yan, Q.J., Rammal, M., Tranfaglia, M., Bauchwitz, R.P.·2005·Neuropharmacology

DOI 10.1016/j.neuropharm.2005.06.004

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Abstract

Fragile X Syndrome is the most common form of inherited mental retardation worldwide. A Fragile X mouse model, fmr1(tm1Cgr), with a disruption in the X-linked Fmr1 gene, has three substantial deficits observed in several strains: (1) sensitivity to audiogenic seizures (AGS), (2) tendency to spend significantly more time in the center of an open field, and (3) enlarged testes. Alterations in metabotropic glutamate receptor group I signaling were previously identified in the fmr1(tm1Cgr) mouse. In this study, we examined the effect of MPEP, an antagonist of the group I metabotropic glutamate receptor mGluR5, on audiogenic seizures and open field activity of fmr1(tm1Cgr) mice. Genetic analysis revealed synergistic reactions between fmr1(tm1Cgr) and inbred AGS alleles. In addition, AGS sensitivity due to the fmr1(tm1Cgr) allele was restricted during development. Examination of phenotypes combining mGluR5 inhibition and Fmr1 mutation indicated that absence of FMRP may affect mGluR5 signaling through indirect as well as direct pathways. All strains of fmr1(tm1Cgr) mice tested (FVB/NJ, C57BL/6J, and an F1 hybrid of the two) had a more excitable AGS pathway than wild-type, and consequently required more MPEP to achieve seizure suppression. At high doses of mGluR5 antagonists, a Fragile X specific tolerance (loss of drug activity) was observed. The tolerance effect could be overcome by a further increase in drug dose. In open field tests, MPEP reduced fmr1(tm1Cgr) center field behavio…

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Authors: Yan, Q. J., Rammal, M., Tranfaglia, M., & Bauchwitz, R. P.
Affiliations: Columbia University (US)
Fraxa Research Foundation (US)
Corresponding author: Bauchwitz, R.P.
ORCID: Bauchwitz, R.P.
Venue: Neuropharmacology
Publisher: Elsevier BV
Published: 2005-12
Volume: 49
Issue: 7
Pages: 1053-1066
ISSN: 0028-3908 (ISSN-L)
DOI: 10.1016/j.neuropharm.2005.06.004
OpenAlex: W2094993063
Cited by: 521
References: 60
Citations by year: 2026: 6 · 2025: 7 · 2024: 8 · 2023: 10 · 2022: 12 · 2021: 16 · 2020: 13 · 2019: 10 · 2018: 12 · 2017: 28 · 2016: 26 · 2015: 26 · 2014: 30 · 2013: 45 · 2012: 47
FWCI: 13.31
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
Locations: Neuropharmacology (publishedVersion)
PubMed (publishedVersion)
CogPrints (University of Southampton) (submittedVersion)
Funders: FRAXA Research Foundation
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Health Sciences › Medicine › Clinical Neurology › Epilepsy research and treatment
Keywords: fragile X syndrome, FMR1 gene, mGluR5, MPEP, audiogenic seizures, testicular enlargement, FMRP, drug tolerance, seizure susceptibility, mouse model
MeSH terms: Aging, Alleles, Animals, Drug Synergism, Exploratory Behavior, Female, Fragile X Syndrome, Genotype, Male, Mice, Inbred C57BL, Phenotype, Pyridines, Receptors, Metabotropic Glutamate, Epilepsy, Reflex, Mice, Fragile X Messenger Ribonucleoprotein 1, Receptor, Metabotropic Glutamate 5

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Suppression of two major Fragile X Syndrome mouse model phenotypes by the mGluR5 antagonist MPEP

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