{"title":"口腔黏膜炎症刺激诱发三叉神经尾侧亚核小胶质细胞的活化。","authors":"Hung-Chih Huang, Michiko Nakatsuka, Yasutomo Iwai","doi":"10.2535/ofaj.89.137","DOIUrl":null,"url":null,"abstract":"<p><p>To study the inflammatory hyperplasia induced by an acute noxious stimulation of oral mucosa with 5% formalin (5%FOR), we performed an immunohistochemical study on the expression of TNFá in the intermolar region of the dorsal lingual eminence (IDLE), and Iba1 and phosphorylated (phospho)- p38 MAPK involved with central nervous system microglial activation in the trigeminal subnucleus caudalis (Vc). The present study observed significantly increased expression of TNFá at either 1h or 24h of 5%FOR nociception, as well as sustained TNFá immunoreactivity in the IDLE. On the other hand, at either 1h or 24h 5%FOR nociception, Iba1- immunoreactive (IR) cells in the Vc were significantly increased after inflammatory stimulation of the IDLE; the increase was more evident at 24h 5%FOR nociception. By using the double-label immunofluorescence technique, the findings in particular demonstrated a significant increase in the number of phospho-p38 MAPK- and Iba1-IR coexpressed cells in the Vc at 24h 5%FOR nociception. The results suggest that 24h persistent microglial activation in subnuclei zonalis and gelatinosus of the Vc is evoked by 5%FOR noxious stimulation of the IDLE oral mucosa, thereby the present study indicates that the MAPK expression plays important roles in microglial activation related with central sensitization and inflammatory hyperalgesia.</p>","PeriodicalId":19462,"journal":{"name":"Okajimas folia anatomica Japonica","volume":"89 4","pages":"137-45"},"PeriodicalIF":0.0000,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2535/ofaj.89.137","citationCount":"7","resultStr":"{\"title\":\"Activation of microglial cells in the trigeminal subnucleus caudalis evoked by inflammatory stimulation of the oral mucosa.\",\"authors\":\"Hung-Chih Huang, Michiko Nakatsuka, Yasutomo Iwai\",\"doi\":\"10.2535/ofaj.89.137\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>To study the inflammatory hyperplasia induced by an acute noxious stimulation of oral mucosa with 5% formalin (5%FOR), we performed an immunohistochemical study on the expression of TNFá in the intermolar region of the dorsal lingual eminence (IDLE), and Iba1 and phosphorylated (phospho)- p38 MAPK involved with central nervous system microglial activation in the trigeminal subnucleus caudalis (Vc). The present study observed significantly increased expression of TNFá at either 1h or 24h of 5%FOR nociception, as well as sustained TNFá immunoreactivity in the IDLE. On the other hand, at either 1h or 24h 5%FOR nociception, Iba1- immunoreactive (IR) cells in the Vc were significantly increased after inflammatory stimulation of the IDLE; the increase was more evident at 24h 5%FOR nociception. By using the double-label immunofluorescence technique, the findings in particular demonstrated a significant increase in the number of phospho-p38 MAPK- and Iba1-IR coexpressed cells in the Vc at 24h 5%FOR nociception. The results suggest that 24h persistent microglial activation in subnuclei zonalis and gelatinosus of the Vc is evoked by 5%FOR noxious stimulation of the IDLE oral mucosa, thereby the present study indicates that the MAPK expression plays important roles in microglial activation related with central sensitization and inflammatory hyperalgesia.</p>\",\"PeriodicalId\":19462,\"journal\":{\"name\":\"Okajimas folia anatomica Japonica\",\"volume\":\"89 4\",\"pages\":\"137-45\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2013-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.2535/ofaj.89.137\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Okajimas folia anatomica Japonica\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2535/ofaj.89.137\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Okajimas folia anatomica Japonica","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2535/ofaj.89.137","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Activation of microglial cells in the trigeminal subnucleus caudalis evoked by inflammatory stimulation of the oral mucosa.
To study the inflammatory hyperplasia induced by an acute noxious stimulation of oral mucosa with 5% formalin (5%FOR), we performed an immunohistochemical study on the expression of TNFá in the intermolar region of the dorsal lingual eminence (IDLE), and Iba1 and phosphorylated (phospho)- p38 MAPK involved with central nervous system microglial activation in the trigeminal subnucleus caudalis (Vc). The present study observed significantly increased expression of TNFá at either 1h or 24h of 5%FOR nociception, as well as sustained TNFá immunoreactivity in the IDLE. On the other hand, at either 1h or 24h 5%FOR nociception, Iba1- immunoreactive (IR) cells in the Vc were significantly increased after inflammatory stimulation of the IDLE; the increase was more evident at 24h 5%FOR nociception. By using the double-label immunofluorescence technique, the findings in particular demonstrated a significant increase in the number of phospho-p38 MAPK- and Iba1-IR coexpressed cells in the Vc at 24h 5%FOR nociception. The results suggest that 24h persistent microglial activation in subnuclei zonalis and gelatinosus of the Vc is evoked by 5%FOR noxious stimulation of the IDLE oral mucosa, thereby the present study indicates that the MAPK expression plays important roles in microglial activation related with central sensitization and inflammatory hyperalgesia.