{"created":"2023-06-20T15:47:28.134828+00:00","id":2009,"links":{},"metadata":{"_buckets":{"deposit":"63bc5f29-570f-4618-8110-c5440953689f"},"_deposit":{"created_by":2,"id":"2009","owners":[2],"pid":{"revision_id":0,"type":"depid","value":"2009"},"status":"published"},"_oai":{"id":"oai:hama-med.repo.nii.ac.jp:00002009","sets":["1:11"]},"author_link":["5208"],"item_3_biblio_info_5":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2006-04-30","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"1","bibliographicPageEnd":"17","bibliographicPageStart":"3","bibliographicVolumeNumber":"24","bibliographic_titles":[{"bibliographic_title":"てんかん研究"}]}]},"item_3_description_9":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"「細胞内Cl^-濃度([Cl^-]_i)は従来考えられていたほど'静的'でなく、種々のCl^-トランスポーターの作用により能動的に変化し、抑制性神経伝達物質GABA(γ-aminobutyric acid)のシナプス後膜GABA_A受容体-Cl^-チャンネルを介する作用を抑制から興奮までダイナミックに変化させて神経回路の機能と形成に関わる」という新しい概念(能動的Cl^-ホメオスタシス仮説)を、実験的てんかん病態モデルで検証してきた。ラット海馬の急性実験では入力線維の高頻度刺激によるGABA_A受容体チャネルからの急激なCl^-流入が[Cl^-]_iの過剰な上昇を招き、その結果GABA作用が抑制から興奮へ逆転して、てんかん発作波様の後発射の引き金となった。慢性のキンドリングモデルでは、海馬や梨状葉皮質で取込型Cl^-トランスポーターのNKCClが有意に増加し、[Cl^-]_iが慢性的に上昇することが示唆された。一方、発達初期ではNKCClによって[Cl^-]_iが高く維持され、GABAがCl^-流出による脱分極で興奮性に作用して神経回路形成に関与するので、[Cl^-]_iの異常が皮質形成異常を誘発する可能性がある。ラットの限局性皮質形成異常モデルでのmicrogyrus形成過程で、NKCClの増加と排出型Cl^-トランスポーターKCC2の減少による[Cl^-]_i上昇と、GABAの抑制から興奮への変化が見られた。以上から、Cl^-ホメオスタシスの異常がてんかん発作の機能的な原因や増悪因子となったり、器質的なてんかん原性の成因とも関わる可能性がある。","subitem_description_type":"Abstract"}]},"item_3_publisher_6":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"日本てんかん学会"}]},"item_3_relation_28":{"attribute_name":"出版社DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"10.3805/jjes.24.3","subitem_relation_type_select":"DOI"}}]},"item_3_rights_7":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"© 日本てんかん学会"}]},"item_3_source_id_19":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"09120890","subitem_source_identifier_type":"ISSN"}]},"item_3_version_type_32":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"福田, 敦夫"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2018-08-27"}],"displaytype":"detail","filename":"Tenkan-24-3.pdf","filesize":[{"value":"1.8 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"Tenkan-24-3.pdf","url":"https://hama-med.repo.nii.ac.jp/record/2009/files/Tenkan-24-3.pdf"},"version_id":"6586e732-b520-43b2-8e4f-6f3decee6a27"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"chloride","subitem_subject_scheme":"Other"},{"subitem_subject":"GABA","subitem_subject_scheme":"Other"},{"subitem_subject":"epilepsy","subitem_subject_scheme":"Other"},{"subitem_subject":"inhibition","subitem_subject_scheme":"Other"},{"subitem_subject":"transporter","subitem_subject_scheme":"Other"}]},"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":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"能動的Cl－ホメオスタシス仮説と実験的てんかん病態モデル","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"能動的Cl－ホメオスタシス仮説と実験的てんかん病態モデル"}]},"item_type_id":"3","owner":"2","path":["11"],"pubdate":{"attribute_name":"公開日","attribute_value":"2013-08-27"},"publish_date":"2013-08-27","publish_status":"0","recid":"2009","relation_version_is_last":true,"title":["能動的Cl－ホメオスタシス仮説と実験的てんかん病態モデル"],"weko_creator_id":"2","weko_shared_id":-1},"updated":"2023-06-20T17:24:13.479982+00:00"}