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利用小鼠模式研究慢性疼痛對於腸道菌群結構與其穩定性之影響

為了解決AIMP的問題，作者蒙國杰 這樣論述：

The gut microbiota, a complicated and highly dynamic ecosystem, consists of microorganisms that live within the gastrointestinal tract of its hosts and its structure and stability is relevant to the host health. The gut-brain axis of vertebrates is a bi-directional integrated system composed by imm

une, endocrine, and neuronal components by which the knowledge regarding the interactions between the gut microbiota and the nervous system (e.g., brain) is lacking. For example, the influence of chronic muscle pain with or without peripheral nerve injury on gut microbiota has not been extensively a

ddressed. Here we used spared-nerve injury (SNI) model that mimics neuropathic pain and acid-induced muscle pain (AIMP) model that mimics fibromyalgia to investigate the link between chronic muscle pain and the dynamics of gut microbiota in C57BL/6 mice. We cut the peripheral nerves for SNI model an

d performed repeated muscle insult on the left gastrocnemius muscle using acidic saline for AIMP model, evaluated with pain behavioral test, and collected multiple fecal samples to generate time-series data. High-throughput amplicon sequencing coupled with mothur identified certain bacteria genera s

uch as Adlercreutzia, Bifidobacterium, Muribacullum, Oscillospira, Staphylococcus, and Erysipelatoclostridium significantly affected by the chronic pain treatments. Microbial interaction network analysis based on generalized Lotka–Volterra (gLV) equations with multiple simulations showed the instabi

lity of gut microbial community when the mice were exhibiting chronic pain. Moreover, the metagenome imputation shed light on the functional profiles of gut microbial communities. Altogether, our bioinformatic analyses of mice gut microbiota indicated the impact of chronic pain on the structure and

stability of gut microbial community in vertebrates.

正常和肌肉痛小鼠在前島腦無顆粒皮質的抑制性中間神經元到第五層錐狀神經元之神經傳導比較

為了解決AIMP的問題，作者林蓓萱 這樣論述：

近期的研究顯示慢性疼痛可能和疼痛相關之大腦核區內的神經興奮性和突觸效力改變有關，即中樞敏感化。前腦島無顆粒皮質(RAIC)被發現在急性和慢性疼痛時都會被活化，且在我們之前的結果中發現肌肉痛小鼠的RAIC裡，神經活性提高的細胞大部分是錐狀細胞，極少數是抑制性中間神經元。因為RAIC中迴路的興奮性突觸訊號和抑制性突觸訊號不平衡會改變其疼痛訊息的輸出，所以此研究目的是比較肌肉痛小鼠和控制組的抑制性中間神經元到錐狀細胞的突觸效力是否不同。我先使用酸誘發肌肉痛模型，讓小鼠的兩隻後腳掌產生痛覺過敏的行為，再進一步用電生理結合光遺傳學的方式檢驗抑制性突觸的傳導。實驗結果顯示慢性疼痛小鼠的抑制性突觸後電流的

paired-pulse ratio顯著地從控制組的0.66減少到0.37，且其突觸傳導的量子大小從控制組的12.88 pA增加到18.82 pA。這意味著在慢性疼痛的形成過程中，RAIC的抑制性中間神經元到第五層錐狀細胞的突觸功能產生變化。