{"created":"2023-07-27T06:44:33.784764+00:00","id":34832,"links":{},"metadata":{"_buckets":{"deposit":"c0726476-ad75-4429-8189-d1108c13f07f"},"_deposit":{"created_by":3,"id":"34832","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"34832"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00034832","sets":["2812:2813:2833"]},"author_link":["253"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2001-03-01","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"4p.","bibliographicVolumeNumber":"1999-2000","bibliographic_titles":[{"bibliographic_title":"平成12(2000)年度 科学研究費補助金 基盤研究(C) 研究成果報告書"},{"bibliographic_title":"2000 Fiscal Year Final Research Report","bibliographic_titleLang":"en"}]}]},"item_9_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{}],"nameIdentifiers":[{},{},{}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"1.ニトリル投与動物における神経毒性発生機序・行動異常発生機序 (1)ニトリル投与動物ではImmediately early gene c-fos産物のFos蛋白質が、前庭神経核を含む若干の神経核に投与1.5時間後から30日後まで免疫組織化学的に確認された。特に30日後までFos発現が認められた神経核は前庭破壊後に観察されるFos発現神経核に一致していたので、ニトリルの前庭傷害作用が推定され行動異常発生との関連が示唆された。 (2)5つのsynaptic marker(γ-aminobutyric acid(GABA),tyrosine hydroxylase(TH),serotonin,serotonin transporter and choline acetyltransferase)の変化を免疫組織化学的に検討した。アリルニトリルは5神経核(medial habenula,interpeduncular nucleus,substantia nigra,dorsal raphe nucleus,median raphe nucleus)にGABA染色性変化をもたらした。GABA染色の程度はmedial habenulaを除くこれらの神経核で投与後2日目で減少し、全ての5神経核で14日目で増加していた。アリルニトリルはまたarcuate nucleus,substantia nigra pars compacta,locus coeruleus,caudoventrolateral reticular nucleusに投与後2日目あるいは14日目でTH染色性変化をもたらした。これらの結果からmedial habenula-interpeduncular nucleus-raphe nuclei路とsubstantia nigraを介したGABA系の異常と行動異常との関連が示唆された。 2.培養PC12細胞におけるアポトーシスカスケードの解析 アリルニトリル(5mM)は培養12時間後に核濃縮とDNAの断片化をもたらした。ヘキスト33258染色で評価された、アリルニトリル誘発性アポトーシスはcaspase-3阻害剤で抑制された。アポトーシス出現に一致して、caspase-3活性の増加、活性型caspase-3(p17)の増加、ミトコンドリアからのcytochromecの遊離の増加、内在性caspase-3の基質poly(ADP-ribose)polymeraseの分解の増加が確認された。これらの結果からアリルニトリルはcytochrome c-caspase-3経路を介してアポトーシスをもたらすことが示された。今後、cytochrome cの遊離を調節するbcl-2familyに焦点をあてた研究が必要である。","subitem_description_type":"Abstract"},{"subitem_description":"(1) The expression of Fos protein was examined within various brain structures in allylnitrile-, crotononitrile-, and vehicle-treated mice. In each nitrile-treated mouse, Fos expression was observed in brain structures, which were divided into two groups. The structures in group 1 showed Fos expression between 1.5 h and 2 days postdosings, and in those in group 2 expression remained for up to 30 days postdosing. The results indicate that each nitrile induces Fos expression by causing a change in the peripheral vestibular system, resulting in behavioral abnormalities.\n(2) Five neuronal markers, γ-aminobutyric acid (GABA), tyrosine hydroxylase, serotorain, the serotonin transporter and choline acetyltransferase were immunohistochemically examined within various brain structures in allylnitrile and vehicle-treated mice. Allylnitrile induced changes in the immunolabelling of GABA in the medial habenula, interpedunculat nucleus, substantia nigra, dorsal raphe nucleus and median raphe nucleus. The results suggest that the GABA ergic systems through the medial habenula-interpeduncular nucleus-ascending rap he nuclei relay and through the substantia nigra may be involved in allylnitrile-induced behavioral abnormalities.\n2.Apoptotic pathway in allylnitrile-treated PC12 cells\nTreatment of differentiated PC12 cells with 5 mM allylnitrile (for up to 12 h) caused nuclear condensation and DNA fragmentation. Allylnitrile-induced apoptosis could be inhibited with the caspase inhibitor. Allylnitrile induced a time-dependentincrease in caspase-3 activity in differentiated cells. Caspase-3 cleavage, cytochromec release from mitochondria and poly (ADP-ribose) polymerase degradation were observed during allylnitrile-induced apoptosis. The results indicate that allylnitrile induces apoptosis through cytochrome c-caspase-3 path way in differentiated PC12 cells.","subitem_description_type":"Abstract"}]},"item_9_description_22":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究課題/領域番号:11670340, 研究期間(年度):1999–2000","subitem_description_type":"Other"},{"subitem_description":"出典：「行動異常誘発性ニトリル中毒マウスでの中枢神経系のアポトーシスと行動との関連」研究成果報告書　課題番号11670340\n(KAKEN：科学研究費助成事業データベース（国立情報学研究所）)\n　　　本文データは著者版報告書より作成","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00034819","subitem_identifier_reg_type":"JaLC"}]},"item_9_publisher_17":{"attribute_name":"公開者","attribute_value_mlt":[{"subitem_publisher":"金沢大学医学部"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=90110618","subitem_relation_type_select":"URI"}},{"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11670340/","subitem_relation_type_select":"URI"}},{"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-11670340/116703402000kenkyu_seika_hokoku_gaiyo/","subitem_relation_type_select":"URI"}}]},"item_9_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-10-05"}],"displaytype":"detail","filename":"ME-PR-TANII-H-kaken 2001-4p.pdf","filesize":[{"value":"129.3 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"ME-PR-TANII-H-kaken 2001-4p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/34832/files/ME-PR-TANII-H-kaken 2001-4p.pdf"},"version_id":"f9f2453c-b766-4ffd-a7fc-ab154ea66c2a"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"行動異常誘発性ニトリル中毒マウスでの中枢神経系のアポトーシスと行動との関連","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"行動異常誘発性ニトリル中毒マウスでの中枢神経系のアポトーシスと行動との関連"},{"subitem_title":"Behavioral abnormalities and apoptotic changes in the nervous system in nitriletreated mice","subitem_title_language":"en"}]},"item_type_id":"9","owner":"3","path":["2833"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-10-05"},"publish_date":"2017-10-05","publish_status":"0","recid":"34832","relation_version_is_last":true,"title":["行動異常誘発性ニトリル中毒マウスでの中枢神経系のアポトーシスと行動との関連"],"weko_creator_id":"3","weko_shared_id":3},"updated":"2023-07-27T14:46:06.139201+00:00"}