Cited by 485Ion channel regulation and functionEpilepsy research and treatmentIon Channels and Receptors

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Ataxia and epileptic seizures in mice lacking type 1 inositol 1,4,5-trisphosphate receptor

Matsumoto, M., Nakagawa, T., Inoue, T., Nagata, E., Tanaka, K., Takano, H., Kuno, J., Sakakibara, S., Yamada, M., Yoneshima, H., Miyawaki, A., Furuichi, Y., Okano, H., Mikoshiba, S. K., Noda, T.·1996·Nature

DOI 10.1038/379168a0

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Abstract

The inositol 1,4,5-trisphosphate (InsP3) receptor acts as an InsP3-gated Ca2+ release channel in a variety of cell types. Type 1 InsP3 receptor (IP3R1) is the major neuronal member of the IP3R family in the central nervous system, predominantly enriched in cerebellar Purkinje cells but also concentrated in neurons in the hippocampal CA1 region, caudate-putamen, and cerebral cortex. Here we report that most IP3R1-deficient mice generated by gene targeting die in utero, and born animals have severe ataxia and tonic or tonic-clonic seizures and die by the weaning period. An electroencephalogram showed that they suffer from epilepsy, indicating that IP3R1 is essential for proper brain function. However, observation by light microscope of the haematoxylin-eosin staining of the brain and peripheral tissues of IP3R1-deficient mice showed no abnormality, and the unique electrophysiological properties of the cerebellar Purkinje cells of IP3R1-deficient mice were not severely impaired.

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Authors: Matsumoto, M., Nakagawa, T., Inoue, T., Nagata, E., Tanaka, K., Takano, H., Kuno, J., Sakakibara, S., Yamada, M., Yoneshima, H., Miyawaki, A., Furuichi, Y., Okano, H., Mikoshiba, S. K., & Noda, T.
Affiliations: Japanese Foundation For Cancer Research (JP)
Institute of Medical Science, The University of Tokyo (JP)
Keio University (JP)
University of Tsukuba (JP)
RIKEN (JP)
ORCID: Matsumoto, M.
Nakagawa, T.
Inoue, T.
Nagata, E.
Tanaka, K.
Takano, H.
Sakakibara, S.
Yamada, M.
Miyawaki, A.
Okano, H.
Noda, T.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 1996-01
Volume: 379
Issue: 6561
Pages: 168-171
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/379168a0
OpenAlex: W2066261176
Cited by: 485
References: 27
Citations by year: 2026: 7 · 2025: 10 · 2024: 6 · 2023: 8 · 2022: 8 · 2021: 12 · 2020: 16 · 2019: 8 · 2018: 14 · 2017: 15 · 2016: 18 · 2015: 10 · 2014: 18 · 2013: 17 · 2012: 21
FWCI: 15.15
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Health Sciences › Medicine › Clinical Neurology › Epilepsy research and treatment
Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords: IP3 receptor, IP3R1, ataxia, epileptic seizures, Purkinje cells, neuronal calcium signaling, developmental lethality, tonic-clonic seizures
MeSH terms: Animals, Ataxia, Base Sequence, Brain, Cell Line, Electroencephalography, Epilepsy, Fetal Death, Molecular Sequence Data, Mutation, Purkinje Cells, Calcium Channels, Inositol 1,4,5-Trisphosphate, DNA Primers, Receptors, Cytoplasmic and Nuclear, Gene Targeting, Mice, Inositol 1,4,5-Trisphosphate Receptors

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Ataxia and epileptic seizures in mice lacking type 1 inositol 1,4,5-trisphosphate receptor

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