{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360004235508768896.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1111/ejn.12891"}},{"identifier":{"@type":"URI","@value":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fejn.12891"}},{"identifier":{"@type":"URI","@value":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/ejn.12891"}},{"identifier":{"@type":"PMID","@value":"25851080"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Changes in hippocampal synaptic functions and protein expression in monosodium glutamate‐treated obese mice during development of glucose intolerance"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title><jats:p>Glucose is the sole neural fuel for the brain and is essential for cognitive function. Abnormalities in glucose tolerance may be associated with impairments in cognitive function. Experimental obese model mice can be generated by an intraperitoneal injection of monosodium glutamate (<jats:styled-content style=\"fixed-case\">MSG</jats:styled-content>; 2 mg/g) once a day for 5 days from 1 day after birth. <jats:styled-content style=\"fixed-case\">MSG</jats:styled-content>‐treated mice have been shown to develop glucose intolerance and exhibit chronic neuroendocrine dysfunction associated with marked cognitive malfunctions at 28–29  weeks old. Although hippocampal synaptic plasticity is impaired in <jats:styled-content style=\"fixed-case\">MSG</jats:styled-content>‐treated mice, changes in synaptic transmission remain unknown. Here, we investigated whether glucose intolerance influenced cognitive function, synaptic properties and protein expression in the hippocampus. We demonstrated that <jats:styled-content style=\"fixed-case\">MSG</jats:styled-content>‐treated mice developed glucose intolerance due to an impairment in the effectiveness of insulin actions, and showed cognitive impairments in the Y‐maze test. Moreover, long‐term potentiation (<jats:styled-content style=\"fixed-case\">LTP</jats:styled-content>) at Schaffer collateral–<jats:styled-content style=\"fixed-case\">CA</jats:styled-content>1 pyramidal synapses in hippocampal slices was impaired, and the relationship between the slope of extracellular field excitatory postsynaptic potential and stimulus intensity of synaptic transmission was weaker in <jats:styled-content style=\"fixed-case\">MSG</jats:styled-content>‐treated mice. The protein levels of vesicular glutamate transporter 1 and GluA1 glutamate receptor subunits decreased in the <jats:styled-content style=\"fixed-case\">CA</jats:styled-content>1 region of <jats:styled-content style=\"fixed-case\">MSG</jats:styled-content>‐treated mice. These results suggest that deficits in glutamatergic presynapses as well as postsynapses lead to impaired synaptic plasticity in <jats:styled-content style=\"fixed-case\">MSG</jats:styled-content>‐treated mice during the development of glucose intolerance, though it remains unknown whether impaired <jats:styled-content style=\"fixed-case\">LTP</jats:styled-content> is due to altered inhibitory transmission. It may be important to examine changes in glucose tolerance in order to prevent cognitive malfunctions associated with diabetes.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380579812378463745","@type":"Researcher","foaf:name":[{"@value":"Sachie Sasaki‐Hamada"}],"jpcoar:affiliationName":[{"@value":"Laboratory of Pharmacology Faculty of Pharmaceutical Sciences Tokyo University of Science 2641 Yamazaki Noda Chiba 278‐8510 Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004235508768771","@type":"Researcher","foaf:name":[{"@value":"Yuki Hojo"}],"jpcoar:affiliationName":[{"@value":"Laboratory of Pharmacology Faculty of Pharmaceutical Sciences Tokyo University of Science 2641 Yamazaki Noda Chiba 278‐8510 Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004235508768769","@type":"Researcher","foaf:name":[{"@value":"Hajime Koyama"}],"jpcoar:affiliationName":[{"@value":"Laboratory of Pharmacology Faculty of Pharmaceutical Sciences Tokyo University of Science 2641 Yamazaki Noda Chiba 278‐8510 Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004235508768651","@type":"Researcher","foaf:name":[{"@value":"Hayuma Otsuka"}],"jpcoar:affiliationName":[{"@value":"Laboratory of Pharmacology Faculty of Pharmaceutical Sciences Tokyo University of Science 2641 Yamazaki Noda Chiba 278‐8510 Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380579812378463744","@type":"Researcher","foaf:name":[{"@value":"Jun‐Ichiro Oka"}],"jpcoar:affiliationName":[{"@value":"Laboratory of Pharmacology Faculty of Pharmaceutical Sciences Tokyo University of Science 2641 Yamazaki Noda Chiba 278‐8510 Japan"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"0953816X"},{"@type":"EISSN","@value":"14609568"}],"prism:publicationName":[{"@value":"European Journal of Neuroscience"}],"dc:publisher":[{"@value":"Wiley"}],"prism:publicationDate":"2015-04-08","prism:volume":"41","prism:number":"11","prism:startingPage":"1393","prism:endingPage":"1401"},"reviewed":"false","dc:rights":["http://onlinelibrary.wiley.com/termsAndConditions#vor"],"url":[{"@id":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fejn.12891"},{"@id":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/ejn.12891"}],"createdAt":"2015-04-08","modifiedAt":"2023-10-03","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Male","dc:title":"Male"},{"@id":"https://cir.nii.ac.jp/all?q=Mice,%20Inbred%20ICR","dc:title":"Mice, Inbred ICR"},{"@id":"https://cir.nii.ac.jp/all?q=Neuronal%20Plasticity","dc:title":"Neuronal Plasticity"},{"@id":"https://cir.nii.ac.jp/all?q=Hippocampus","dc:title":"Hippocampus"},{"@id":"https://cir.nii.ac.jp/all?q=Synaptic%20Transmission","dc:title":"Synaptic Transmission"},{"@id":"https://cir.nii.ac.jp/all?q=Actins","dc:title":"Actins"},{"@id":"https://cir.nii.ac.jp/all?q=Mice","dc:title":"Mice"},{"@id":"https://cir.nii.ac.jp/all?q=Memory,%20Short-Term","dc:title":"Memory, Short-Term"},{"@id":"https://cir.nii.ac.jp/all?q=Glucose%20Intolerance","dc:title":"Glucose Intolerance"},{"@id":"https://cir.nii.ac.jp/all?q=Sodium%20Glutamate","dc:title":"Sodium Glutamate"},{"@id":"https://cir.nii.ac.jp/all?q=Vesicular%20Glutamate%20Transport%20Protein%201","dc:title":"Vesicular Glutamate Transport Protein 1"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=Female","dc:title":"Female"},{"@id":"https://cir.nii.ac.jp/all?q=Obesity","dc:title":"Obesity"},{"@id":"https://cir.nii.ac.jp/all?q=Receptors,%20AMPA","dc:title":"Receptors, AMPA"},{"@id":"https://cir.nii.ac.jp/all?q=Maze%20Learning","dc:title":"Maze Learning"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040000781848604160","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"15K07974"},{"@type":"JGN","@value":"JP15K07974"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15K07974/"}],"notation":[{"@language":"ja","@value":"中枢作用性ペプチド製剤の開発と経鼻投与による臨床応用に向けた薬理学的基盤研究"},{"@language":"en","@value":"Pharmacological and translational studies of centrally-acting peptide derivatives specialized in the delivery to the brain by the intranasal administration"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360011143656749184","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Behavioural studies in rats treated with monosodium l-glutamate during the early stages of life"}]},{"@id":"https://cir.nii.ac.jp/crid/1360011145447651200","@type":"Article","relationType":["references"],"jpcoar:relatedTitle":[{"@value":"Deficit in hippocampal long-term potentiation in 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