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解析下視丘投射至海馬回突觸中共同傳遞麩胺酸及-氨基丁酸的功能意義

為了解決Tp link PTT的問題，作者伊木夏 這樣論述：

中文摘要海馬回為負責認知及情緒功能的關鍵腦區。齒狀回為海馬回次核區中的第一個訊號處理器其會接受來自大腦皮質及皮質下核區傳來的訊號。其中，大腦皮質至海馬回路徑會在記憶獲得及提取時傳遞記憶相關的訊息；然而，來自皮質下的訊號參與了調控皮質及海馬回間的訊息溝通。下視丘乳頭上核藉由共同釋放兩種截然不同的快速神經傳遞物質，也就是麩胺酸及-氨基丁酸，來實質上的支配齒狀回活性，因而能協助空間定位及空間記憶的形成。然而乳頭上核中神經元是藉由何種突觸機制來調控齒狀回活性及其突觸可塑性尚未被釐清。齒狀回由興奮性的顆粒細胞及抑制性的中間神經元所組成。在這本論文中，我用光遺傳學、電生理及藥理學的方法，證明來自乳頭上

核的訊號會透過不同的突觸機制差異性地調控齒狀回中不同種細胞的活性。選擇性活化乳頭上核會在所有的突觸後神經元產生突觸興奮及突觸抑制作用，然而這兩種作用的比例是會依突觸後細胞種類的不同而改變的。具體來說，樹突抑制型中間神經元主要接收突觸興奮作用，然而體抑制型中間神經元及顆粒細胞則主要接收突觸抑制訊號。雖然單獨活化乳頭上核並不足以興奮顆粒細胞，但是在有興奮性驅動力的情況下，活化乳頭上核可使顆粒細胞產生動作電位的時間更精準並縮短其產生動作電位所需的時間。此外，在有皮質訊號輸入時活化乳頭上核會增加顆粒細胞動作電位的產生，進而促使皮質到顆粒細胞突觸間的長期增強作用。總結來說，這些發現顯示了乳頭上核共同傳遞

的麩胺酸及-氨基丁酸對於維持齒狀回中興奮/抑制的動態平衡是有貢獻的，並且能透過提升皮質到顆粒細胞突觸間的長期增強作用來幫助記憶的編碼。

Snail上調FN, LEF, COX2 及 COL1A1基因的分子機轉: Snail轉錄活化間質蛋白的共同模式之建立

為了解決Tp link PTT的問題，作者Ly Minh Tam 這樣論述：

Hepatocellular carcinoma (HCC) progression involves a mechanism known as epithelial mesenchymal transition (EMT). Snail (SNA) is one of the most important transcription factors in EMT because it has the ability to decrease epithelial genes while upregulating mesenchymal genes. Nevertheless, the pro

cesses by which SNA transactivates mesenchymal markers remain unknown. Previously, we established that SNA works in collaboration with SP1 and EGR1 to directly induce ZEB1 and MMP9 transcription. Surprisingly, upstream of the EGR/SP1 overlapping area on promoters, a SNA-binding motif (TCACA) was dis

covered. Hence, the point of this research was to identify whether SNA similarly upregulates four other mesenchymal genes: fibronectin (FN), lymphoid enhancer-binding factor (LEF), collagen type alpha I (COL1A1), and cyclooxygenase 2 (COX2). SNA, as expected, is required for the activity of these me

senchymal markers. By using deletion mapping and site directed mutagenesis in combination with a dual luciferase promoter assay, it was found that the SNA-binding motif and the EGR1/SP1 overlapping area are necessary for transcription of FN, LEF, COL1A1, and COX2 genes elicited by the phorbol ester

tumor promoter 12-O-tetradecanoyl-phorbol 13-acetate (TPA) in HCC340 and HepG2 HCC cells. Furthermore, using ChIP and EMSA, TPA consistently promoted SNA and EGR1/SP1 binding to these mesenchymal genes' key promoter regions. So far, we've determined that six mesenchymal markers are activated by SNA

in the same transcriptional manner. Likewise, a systematic screening exhibited similar sequence structures in the promoter areas of other SNA-induced mesenchymal genes, implying the possibility of developing a universal model for SNA-induced mesenchymal genes. In conclusion, we hypothesized a novel

mechanism by which Snail acts as a positive transcriptional regulatory factor essential for EMT and metastasis of HCC.Keywords: snail, lymphoid enhancer-binding factor, fibronectin, collagen type alpha I, cyclooxygenase 2, HCC, transcription.