{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,14]],"date-time":"2025-05-14T01:48:12Z","timestamp":1747187292351,"version":"3.40.5"},"reference-count":53,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2019,12,2]],"date-time":"2019-12-02T00:00:00Z","timestamp":1575244800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003478","name":"Ministry of Health, Labour and Welfare","doi-asserted-by":"publisher","award":["H29\u2010Shokuhin\u2010Ippan\u2010004"],"award-info":[{"award-number":["H29\u2010Shokuhin\u2010Ippan\u2010004"]}],"id":[{"id":"10.13039\/501100003478","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Neuropathology"],"published-print":{"date-parts":[[2020,4]]},"abstract":"<jats:p>The cerebellar lesions of bovine spongiform encephalopathy (BSE)\u2010infected guinea pigs were characterized as severe atrophy of the cerebellar cortex associated with the loss of granule cells, decrease in the width of the molecular layer, and intense protease\u2010resistant prion protein (PrP<jats:sup>Sc<\/jats:sup>) accumulations that are similar to cerebellar lesions in kuru and the VV2 type of sporadic Creutzfeldt\u2010Jakob disease. The aim of this study is to assess the relationships between the distribution and localization of PrP<jats:sup>Sc<\/jats:sup>and synapses expressing neurotransmitter transporters in order to reveal the pathogenesis of the disease. We used cell\u2010type\u2010specific immunohistochemical makers recognizing glutamatergic and \u03b3\u2010aminobutylic acid (GABA)ergic terminals to identify terminals impaired with PrP<jats:sup>Sc<\/jats:sup>accumulations. The distribution of PrP<jats:sup>Sc<\/jats:sup>accumulations and immunoreactivity of synaptic vesicles were studied throughout the neuroanatomical pathways in cerebellar lesions. Time course study demonstrated that PrP<jats:sup>Sc<\/jats:sup>accumulation showed a tendency to spread from granular layer to molecular layer. The immunoreactivity of vesicular glutamate transporter 1 (VGluT1) was localized in axon terminals of cerebellar granule cells, and decreased in association with the severity of PrP<jats:sup>Sc<\/jats:sup>accumulations and loss of granule cells. Immunoreactivities of vesicular glutamate transporter 2 (VGluT2) and vesicular GABA transporter (VGAT) that exist in axon terminals of inferior olivary neurons and GABAergic synapses of Purkinje cells, respectively, were preserved well in these lesions. In brainstem, VGluT1 immunoreactivity decreased selectively in pontine nuclei that are a component of the pontocerebellar pathway, although other neurotransmitter immunoreactivities were preserved well. Our findings suggest that the selective loss of VGluT1\u2010immunoreactive synapses subsequent to PrP<jats:sup>Sc<\/jats:sup>accumulations can contribute to the pathogenesis of cerebellar lesions of BSE\u2010infected guinea pigs.<\/jats:p>","DOI":"10.1111\/neup.12613","type":"journal-article","created":{"date-parts":[[2019,12,3]],"date-time":"2019-12-03T05:07:53Z","timestamp":1575349673000},"page":"167-179","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Selective neuronal vulnerability is involved in cerebellar lesions of Guinea pigs infected with bovine spongiform encephalopathy (BSE) prions: Immunohistochemical and electron microscopic investigations"],"prefix":"10.1111","volume":"40","author":[{"given":"Shoichi","family":"Sakaguchi","sequence":"first","affiliation":[{"name":"Division of Veterinary Sciences, Department of Veterinary Medicine Obihiro University of Agriculture and Veterinary Medicine Obihiro 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