Absence of metabotropic glutamate receptor-mediated plasticity in the neocortex of fragile X mice.

Absence of metabotropic glutamate receptor-mediated plasticity in the neocortex of fragile X mice. Research Abstract Details 

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Absence of metabotropic glutamate receptor-mediated plasticity in the neocortex of fragile X mice. Abstract Text:

Brian M Wilson,Charles L Cox,

Fragile X syndrome is a common heritable form of mental retardation in humans. Recent neuroanatomical studies indicate an apparent immature appearance of neurons in fragile X syndrome patients and fragile X mental retardation protein (FMRP)-knockout mice, an animal model of this condition. In this work, we investigated possible alterations in synaptic plasticity in the neocortex of FMRP-knockout mice. Extracellular field potentials were recorded from the deep-layer visual neocortex. Long-term potentiation (LTP) was severely attenuated in brain slices from knockout mice relative to that observed in slices from wild-type mice. Considering that neocortical LTP can involve both NMDA receptor-dependent and -independent mechanisms, we attempted to distinguish the nature of LTP attenuated in the knockout condition. In slices from wild-type mice, LTP was partially attenuated by the NMDA receptor antagonist 3-[(+/-)-2-carboxypiperazin-4-yl]-propyl-1-phosphate (CPP); however, the general metabotropic glutamate receptor (mGluR) antagonist alpha-methyl-4-carboxyphenylglycine (MCPG) strongly attenuated LTP, resulting in a response indistinguishable from that observed in slices from knockout mice. The selective mGluR5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) attenuated LTP to a similar degree as did MCPG in wild-type slices, but MPEP did not alter the reduced potentiation in knockout slices. Our results suggest that LTP in layer V visual neocortex depends primarily on mGluR5 activation. Our data also indicate that mGluR5-mediated synaptic plasticity is absent in the neocortex of FMRP-knockout mice. Such an alteration may contribute to the cognitive and learning deficits exhibited in these mice as well as in fragile X syndrome.

Absence of metabotropic glutamate receptor-mediated plasticity in the neocortex of fragile X mice. Publishing Authors By Initials

BM Wilson,CL Cox,

For similar proteins: membrane proteins: receptors, cell surface: receptors, neurotransmitter: receptors, amino acid: receptors, glutamate: receptors, n-methyl-d-aspartate research abstracts see: proteins: membrane proteins: receptors, cell surface: receptors, neurotransmitter: receptors, amino acid: receptors, glutamate: receptors, n-methyl-d-aspartate research

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Absence of metabotropic glutamate receptor-mediated plasticity in the neocortex of fragile X mice. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Proceedings of the National Academy of Sciences of

VOLUME: 104

Page Numbers: 2454-9

Journal Abbreviation: Proc. Natl. Acad. Sci. U.S.A.

ISSN: 0027-8424

DAY: 7

MONTH: 02

YEAR: 2007

Absence of metabotropic glutamate receptor-mediated plasticity in the neocortex of fragile X mice. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7505876

Absence of metabotropic glutamate receptor-mediated plasticity in the neocortex of fragile X mice. Keywords Mesh Terms:

KEYWORDS: Receptors, N-Methyl-D-Aspartate

MESH TERMS: physiology

Chemical & Substance for Abstract: Absence of metabotropic glutamate receptor-mediated plasticity in the neocortex of fragile X mice. Information

Substance Name: Fragile X Mental Retardation Protein

Registry Number: 139135-51-6

Grant and Affiliation Information for Absence of metabotropic glutamate receptor-mediated plasticity in the neocortex of fragile X mice.

AFFILIATION: Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.

Country: United States

AGENCY: United States NEI

GRANT: EY014024

ACRONYM: EY

MEDLINETA: Proc Natl Acad Sci U S A

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