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Loss of M5 muscarinic acetylcholine receptors leads to cerebrovascular and neuronal abnormalities and cognitive deficits in mice.
https://repo.qst.go.jp/records/44855
https://repo.qst.go.jp/records/448557bdb007c-4842-49b6-a46e-1aa42657af56
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2007-05-28 | |||||
タイトル | ||||||
タイトル | Loss of M5 muscarinic acetylcholine receptors leads to cerebrovascular and neuronal abnormalities and cognitive deficits in mice. | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
アクセス権 | ||||||
アクセス権 | metadata only access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
著者 |
Araya, Runa
× Araya, Runa× Noguchi, Takanori× Yuhki, Munehiro× Higuchi, Makoto× Kanno, Iwao× et.al× 樋口 真人× 菅野 巖 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The M5 muscarinic acetylcholine receptor (M5R) has been shown to play a crucial role in mediating acetylcholine-dependent dilation of cerebral blood vessels. We show that male M5R-/- mice displayed constitutive constriction of cerebral arteries using magnetic resonance angiography in vivo. Male M5R-/- mice exhibited a significantly reduced cerebral blood flow (CBF) in the cerebral cortex, hippocampus, basal ganglia, and thalamus. Cortical and hippocampal pyramidal neurons from M5R-/- mice showed neuronal atrophy. Hippocampus-dependent spatial and nonspatial memory was also impaired in M5R-/- mice. In M5R-/- mice, CA3 pyramidal cells displayed a significantly attenuated frequency of the spontaneous postsynaptic current and long-term potentiation was significantly impaired at the mossy fiber-CA3 synapse. Our findings suggest that impaired M5R signaling may play a role in the pathophysiology of cerebrovascular deficits. The M5 receptor may represent an attractive novel therapeutic target to ameliorate memory deficits caused by impaired cerebrovascular function. | |||||
書誌情報 |
Neurobiology of Disease 巻 24, 号 2, p. 334-344, 発行日 2006-11 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0969-9961 |