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カトウ ケイコ
KATO KEIKO
加藤 啓子 所属 京都産業大学 生命科学部 先端生命科学科 職種 教授 |
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| 言語種別 | 英語 |
| 発行・発表の年月 | 2014/12 |
| 形態種別 | その他 |
| 標題 | Sialyltransferase ST3Gal IV deletion protects against temporal lobe epilepsy |
| 執筆形態 | その他 |
| 掲載誌名 | JOURNAL OF NEUROCHEMISTRY |
| 出版社・発行元 | WILEY-BLACKWELL |
| 巻・号・頁 | 131(5),pp.675-687 |
| 著者・共著者 | Paitoon Srimontri,Shogo Endo,Toshiro Sakamoto,Yoshiaki Nakayama,Akira Kurosaka,Shigeyoshi Itohara,Yoshio Hirabayashi,Keiko Kato |
| 概要 | Temporal lobe epilepsy (TLE) often becomes refractory, and patients with TLE show a high incidence of psychiatric symptoms, including anxiety and depression. Therefore, it is necessary to identify molecules that were previously unknown to contribute to epilepsy and its associated disorders. We previously found that the sialyltransferase ST3Gal IV is up-regulated within the neural circuits through which amygdala-kindling stimulation propagates epileptic seizures. In contrast, this study demonstrated that kindling stimulation failed to evoke epileptic seizures in ST3Gal IV-deficient mice. Furthermore, approximately 80% of these mice failed to show tonic-clonic seizures with stimulation, whereas all littermate wild-type mice showed tonic-clonic seizures. This indicates that the loss of ST3Gal IV does not cause TLE in mice. Meanwhile, ST3Gal IV-deficient mice exhibited decreased acclimation in the open field test, increased immobility in the forced swim test, enhanced freezing during delay auditory fear conditioning, and sleep disturbances. Thus, the loss of ST3Gal IV modulates anxiety-related behaviors. These findings indicate that ST3Gal IV is a key molecule in the mechanisms underlying anxiety - a side effect of TLE - and may therefore also be an effective target for treating epilepsy, acting through the same circuits. |
| DOI | 10.1111/jnc.12838 |
| ISSN | 0022-3042/1471-4159 |