移動力是驅使動物從一個地點移動至另一個地點的一種基礎且不可或缺的行為。越來越多的證據指出移動力可以受到腸胃道驅使的動機狀態而觸發，例如食慾及代謝狀態。近期的研究顯示分佈於腸道的迷走神經是將腸胃道中訊息傳至大腦的關鍵途徑。腸激素尤其重要，由於各種不同的腸激素受體分佈在迷走神經末梢並且以突觸連結著腸內分泌細胞。有趣的是，腸激素的濃度可以經由腸道微生物相的定殖狀態所調控，這說明了腸道微生物、腸道激素和大腦之間存在著複雜的交互作用。然而，由腸道微生物相所調節的內分泌訊號對於移動力調控的詳細機制仍不清楚。在此，我的假說為由腸道微生物相所調節的厭食性腸激素胰高血糖素樣肽-1透過迷走神經傳入途徑調控移動力。在我的研究中，擁有完整腸道菌相的無特定病原小鼠在給予胰高血糖素樣肽-1受體的活化劑時會降低其移動力。由於腸道微生物已知可以抑制胰高血糖素樣肽-1的濃度，因此利用廣效型抗生素加入飲水當中給予無特定病原小鼠來清除定殖的腸道微生物。在廣效型抗生素處理小鼠中觀察到移動力低下以及血清中胰高血糖素樣肽-1濃度的上升，且廣效型抗生素處理小鼠移動力低下的表現可經由抑制胰高血糖素樣肽-1的訊號來提升。為了測試迷走神經是否作為廣效型抗生素處理小鼠移動力低下以及胰高血糖素樣肽-1上升的溝通橋樑，而對廣效型抗生素處理小鼠進行了橫膈下方迷走神經切除術。橫膈下方迷走神經切除手術顯著地成功逆轉了廣效型抗生素處理小鼠移動力低下的表現。此外，抑制胰高血糖素樣肽-1的訊號對沒有橫膈下方迷走神經的廣效型抗生素處理小鼠的移動力無法造成影響。而在廣效型抗生素處理小鼠的迷走神經上行至大腦的區域以及迷走神經投射的區域發現了早期立即基因c-Fos（一種與突觸活性相關的轉錄因子）的增加。因此，利用化學遺傳學的方式抑制迷走神經投射的區域杏仁核之中央核興奮性神經元發現了移動力增加。最後，選擇性的抗生素處理大幅地增加了血清中胰高血糖素樣肽-1的濃度，表明了一種特定類別的腸道細菌在調控著胰高血糖素樣肽-1。這些結果強烈地證明了迷走神經在微生物相所調節的腸激素胰高血糖素樣肽-1之訊號及其所調控的移動力是不可或缺的。我們的研究突顯了迷走神經依賴的神經途徑可作為連結腸道與大腦的橋梁，並且接收著依賴微生物相的腸道內分泌以及調控著移動功能。

Locomotor activity is a fundamental and essential behavior that drives animals from one place to another. Accumulating evidence implicates that locomotion can be triggered by gut-driven motivation status, such as appetite and metabolic condition. Recent studies indicated that vagal innervation in the gut is the crucial pathway for signal transduction to the brain. Gut hormones are particularly critical since various receptors for gut hormones distribute in the vagus nerve terminal synaptically connecting the enteroendocrine cells. Interestingly, the levels of gut hormones can be driven by the colonization status of gut microbiota, suggesting a complicated interaction among gut bacteria, gut hormones, and brain. However, the detailed mechanism underlying the gut microbiota-mediated endocrine signaling in the modulation of locomotion is still unclear. Herein, I hypothesized that the anorexigenic gut hormone glucagon-like peptide-1 (GLP-1) mediated by gut microbiota modulates the locomotion through the vagal afferent pathway. In my study, the administration of the GLP-1 receptor agonist in specific-pathogen-free (SPF) mice with intact gut flora reduced their locomotor activity. Since gut microbiota is known to suppress the levels of GLP-1 in the circulation, SPF mice were given the broad-spectrum antibiotic cocktail (ABX) in drinking water to deplete the colonized gut bacteria. The decrease of locomotion phenotype and increase of sera GLP-1 levels were observed in ABX mice. The hypolocomotion phenotype found in ABX mice can be rescued by attenuating GLP-1 signaling. To test whether the vagus nerve bridges the hypolocomotion outcome and GLP-1 upregulation in ABX mice, subdiaphragmatic vagotomy (SDV) procedure was then executed in ABX mice. Strikingly, the SDV procedure successfully reversed the hypolocomotion phenotype observed in ABX mice. In addition, attenuating GLP-1 signaling had no effect on the locomotion in ABX- SDV mice. The immediate early gene c-Fos, a transcriptional factor associated with the synaptic activity, was upregulated in vagal ascending brain regions and vagal projecting areas in ABX mice. Therefore, one vagal projecting area- the excitatory neurons in central amygdala (CeA) was chemogenetically silenced and found increased locomotion. Finally, selective antibiotic treatment dramatically increased the GLP-1 levels in the serum, suggesting a unique gut bacteria taxa in the regulation of GLP-1. These results robustly demonstrated that the vagus nerve is essential for the locomotor activity modulated by microbiota-mediated gut hormone GLP-1 signaling. Our study highlights the significant role of the vagal-dependent neural pathway as a bridge connecting the gut and the brain in the sensation of microbiota-dependent enteroendocrine and the modulation of motor function.

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