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Neurodegeneration in Lurcher mice caused by mutation in δ2 glutamate receptor gene

Zuo, Jian, De Jager, Philip L., Takahashi, Kanji A., Jiang, Weining, Linden, David J., Heintz, Nathaniel·1997·Nature

DOI 10.1038/42009

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Abstract

Lurcher (Lc) is a spontaneous, semidominant mouse neurological mutation. Heterozygous Lurcher mice (Lc/+) display ataxia as a result of a selective, cell-autonomous and apoptotic death of cerebellar Purkinje cells during postnatal development. Homozygous Lurcher mice (Lc/Lc) die shortly after birth because of a massive loss of mid- and hindbrain neurons during late embryogenesis. We have used positional cloning to identify the mutations responsible for neurodegeneration in two independent Lc alleles as G-to-A transitions that change a highly conserved alanine to a threonine residue in transmembrane domain III of the mouse delta2 glutamate receptor gene (GluR delta2). Lc/+ Purkinje cells have a very high membrane conductance and a depolarized resting potential, indicating the presence of a large, constitutive inward current. Expression of the mutant GluR delta2(Lc) protein in Xenopus oocytes confirmed these results, demonstrating that Lc is inherited as a neurodegenerative disorder resulting from a gain-of-function mutation in a glutamate receptor gene. Thus the activation of apoptotic neuronal death in Lurcher mice may provide a physiologically relevant model for excitotoxic cell death.

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Authors: Zuo, J., De Jager, P. L., Takahashi, K. A., Jiang, W., Linden, D. J., & Heintz, N.
Affiliations: Howard Hughes Medical Institute (US)
Johns Hopkins University (US)
Corresponding author: Heintz, Nathaniel
ORCID: Zuo, Jian
Takahashi, Kanji A.
Linden, David J.
Heintz, Nathaniel
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 1997-08-21
Volume: 388
Issue: 6644
Pages: 769-773
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/42009
OpenAlex: W1523646668
Cited by: 554
References: 22
Citations by year: 2026: 5 · 2025: 8 · 2024: 6 · 2023: 12 · 2022: 9 · 2021: 17 · 2020: 18 · 2019: 8 · 2018: 9 · 2017: 9 · 2016: 14 · 2015: 15 · 2014: 20 · 2013: 17 · 2012: 23
FWCI: 12.06
Type: journal article
Language: en
Open access: closed
Licence: www.springernature.com/gp/researchers/text-and-data-mining (tdm)
www.springernature.com/gp/researchers/text-and-data-mining (vor)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
RePEc: Research Papers in Economics (submittedVersion)
Funders: Howard Hughes Medical Institute
American-Scandinavian Foundation
McKnight Foundation
National Fish and Wildlife Foundation
National Alliance for Research on Schizophrenia and Depression
National Institutes of Health
Comisión de Investigaciones Científicas
National Institute of Mental Health (MH 51106)
National Institute of General Medical Sciences
National Marine Fisheries Service
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
Keywords: neurodegeneration, Purkinje cell death, apoptosis, gain-of-function mutations, excitotoxic cell death, cerebellum, ataxia, positional cloning
MeSH terms: Amino Acid Sequence, Animals, Chromosome Mapping, Electrophysiology, Exons, Introns, Mice, Inbred Strains, Mice, Neurologic Mutants, Molecular Sequence Data, Nerve Degeneration, Nervous System Diseases, Purkinje Cells, Recombinant Proteins, Xenopus laevis, Point Mutation, Sequence Homology, Amino Acid, Receptors, Glutamate, Polymorphism, Single-Stranded Conformational, Mice, In Vitro Techniques

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Neurodegeneration in Lurcher mice caused by mutation in δ2 glutamate receptor gene

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