ID | 69263 |
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Author |
Ueno, Hiroshi
Department of Medical Technology, Kawasaki University of Medical Welfare
Takahashi, Yu
Department of Psychiatry, Kawasaki Medical School
Mori, Sachiko
Department of Psychiatry, Kawasaki Medical School
Kitano, Eriko
Department of Psychiatry, Kawasaki Medical School
Murakami, Shinji
Department of Psychiatry, Kawasaki Medical School
Wani, Kenta
Department of Psychiatry, Kawasaki Medical School
Matsumoto, Yosuke
Department of Neuropsychiatry, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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Okamoto, Motoi
Department of Medical Technology, Graduate School of Health Sciences, Okayama University
Kaken ID
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Ishihara, Takeshi
Department of Psychiatry, Kawasaki Medical School
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Abstract | Perineuronal nets (PNNs) form at the end of the critical period of plasticity in the mouse primary somatosensory cortex. PNNs are said to have functions that control neuroplasticity and provide neuroprotection. However, it is not clear which molecules in PNNs have these functions. We have previously reported that Cat-315-positive molecules were not expressed in the PNNs of the senescence-accelerated model (SAM)P10 strain model mice at 12 months of age. To confirm whether the loss of Cat-315-positive molecules occurred early in life in SAMP10 mice, we examined Cat-315-positive PNNs in the primary somatosensory cortex during postnatal development. This research helps to elucidate the function of PNNs and the mechanism of cognitive decline associated with ageing. To confirm whether Cat-315-positive PNNs changed in an age-dependent manner in SAMP10 mice, we examined the primary somatosensory cortex at 21, 28, and 56 days after birth. We compared these results with those of senescence-accelerated mouse-resistant (SAMR) mice. In SAMP10 mice, Cat-315-positive PNNs were expressed in the primary somatosensory cortex early after birth, but their expression was significantly lower than that in SAMR1 mice. Many other molecules that calibrated the PNN were unchanged between SAMP10 and SAMR1 mice. This study revealed that the expression of the Cat-315 epitope was decreased in the primary somatosensory cortex of SAMP10 mice during postnatal development. SAMP10 mice have had histological abnormalities in their brains since early life. Furthermore, using SAMP10 will be useful in elucidating the mechanism of age-related abnormalities in brain function as well as in elucidating the function and structure of PNNs.
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Keywords | Ageing
Brain function
Neuroplasticity
Neuroprotection
Cognitive decline
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Published Date | 2025-06
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Publication Title |
IBRO Neuroscience Reports
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Volume | volume18
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Publisher | Elsevier BV
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Start Page | 244
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End Page | 256
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ISSN | 2667-2421
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Content Type |
Journal Article
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language |
English
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OAI-PMH Set |
岡山大学
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Copyright Holders | © 2025 The Authors.
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File Version | publisher
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Related Url | isVersionOf https://doi.org/10.1016/j.ibneur.2025.01.012
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License | http://creativecommons.org/licenses/by/4.0/
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