@article{oai:mdu.repo.nii.ac.jp:00000087,
 author = {時崎, 匡史 and 奥村, 雅代 and 大木, 絵美 and 岡藤, 範正 and 栗原, 三郎 and 山田, 一尋 and 宇都野, 創 and 田所, 治 and 金銅, 英二},
 issue = {2},
 journal = {松本歯学},
 month = {Aug},
 note = {application/pdf, Allodynia can be induced by transection of the inferior alveolar nerve (IAN). However, even though the transected IAN is a component of the mandibular nerve in the trigeminal ganglion (TG), allodynia developes in the whisker pads, which are innervated by the uninjured infraorbital nerve (ION), a component of the maxillary nerve in the TG. Our microarray analyses have found that many gene expression levels not only in the injured IAN cell bodies, but also in the uninjured neurons were changed by IAN transection. To demonstrate the relationship between gene expression changes in ION neurons and allodynia, we investigated the expression of 22 genes that were up-regulated in the TG ION area containing ION cell bodies in IAN-transected rats. Real-time PCR, in situ hybridization and quantitative PCR analyses indicated that the myelin basic protein (MBP) mRNA was localized to the trigeminal ganglion neurons and that the expression was significantly up-regulated in the ION area of TG after IAN transection. This finding suggests that MBP or myelin sheath in the uninjured neuron plays a role in allodynia onset following nerve injury.},
 pages = {93--106},
 title = {下歯槽神経切断モデルラットにおける三叉神経節非損傷神経の遺伝子発現動態解析 : 感覚異常発生との関連},
 volume = {36},
 year = {2010}
}