本研究重點關注氯胺酮(ketamine，俗稱Ｋ他命)對神經遞質(neurotransmitter)釋放和囊泡(vesicle)融合的影響，及其在憂鬱症治療中的應用。臨床研究顯示，氯胺酮可以快速且有效地緩解憂鬱症狀。目前的研究指出，氯胺酮的藥理治療可能與阻斷神經元(neuron)突觸間隙(synapse)中之谷氨酸(glutamic acid)的再吸收與神經元囊泡之釋放有關，但確切之作用機制仍有待釐清。因此，本研究將透過仿生脂質膜(biomimetic lipid membranes，作為神經元之細胞膜的模型系統)進行物理實驗，包括在膜融合實驗中氯胺酮是否影響融合程度釋放神經傳遞質，以及探討其原因是否為脂質膜的物理性質(脂雙層厚度和自發曲率)的改變，來進一步瞭解氯胺酮緩解憂鬱症狀的藥理機制。氯胺酮的存在對於脂雙層厚度及自發曲率並無太大變化，對於添加氯胺酮後的膜融合程度降低可能有其他原因。;This study focuses on the effects of ketamine on neurotransmitter release and vesicle fusion, and its application in the treatment of depression. Clinical studies show that ketamine can quickly and effectively relieve symptoms of depression. Current research points out that pharmacological treatment with ketamine may be related to blocking the reabsorption of glutamic acid and the release of neuronal vesicles in the synapse of neurons, but the exact mechanism of action Still to be clarified. Therefore, this study will conduct physical experiments through biomimetic lipid membranes (as a model system of neuronal cell membranes), including whether ketamine affects the extent of fusion and the release of neurotransmitters in membrane fusion experiments, and explore whether the reasons are. To further understand the pharmacological mechanism of ketamine in relieving depression symptoms through changes in the physical properties of lipid membranes (lipid bilayer thickness and spontaneous curvature). The presence of ketamine did not change the lipid bilayer thickness and spontaneous curvature much, and there may be other reasons for the reduced extent of membrane fusion after the addition of ketamine.
