帕金森氏症是一種神經退化性疾病，成因為調控運動功能的黑質及尾狀核/殼核末端中多巴胺神經元傳導路徑受損，導致多巴胺分泌不足。左旋多巴胺 （L-DOPA）是一般常見治療帕金森氏症的藥物，用於補足多巴胺濃度，但服用左旋多巴胺6至10年會使患者出現不穩定運動的副作用，稱為左旋多巴胺誘發運動障礙，而先前的研究有發現，D1和D2受體反應的不平衡會導致此副作用。三磷酸腺苷敏感型鉀離子通道表現在許多組織中，其中有包含大腦，且已知此通道會去影響在多巴胺神經中的陣發放電。在實驗室先前的研究已經發現三磷酸腺苷的開放劑Diazoxide在6-羥多巴胺 (6-OHDA)受損所建立的單側帕金森氏症動物模式中可以減緩左旋多巴胺誘發運動障礙。因此，我們想要了解三磷酸腺苷敏感型鉀離子及多巴胺受體如何去影響左旋多巴胺誘發運動障礙及兩者之間的關係，我們發現阻斷劑Glibenclamide增加了在紋狀體中D3受體及Kir6.2的表達量但Diazoxide減少D3受體及Kir6.2，並且在細胞實驗中也發現，處理過D3受體的激動劑後SUR1及Kir6.2的表達量上升。

Parkinson’s disease (PD) is a neurodegenerative disease caused by the loss of dopamine neurons in the nigrostriatal pathway. The projection of this pathway is from the substantia nigra to the dorsal striatum that fine-tunes our movement. The degeneration of this pathway provokes low dopamine that leads to PD’s symptoms. Levodopa (L-DOPA) prescription is the typical therapy for PD patients to increase DA. Unfortunately, when PD patients have taken this medicine for 6 to 10 years, they would have a side effect called L-DOPA-induced dyskinesia (LID). Some studies show that the imbalance of dopamine pathway (D1 and D2 pathway) may cause LID. KATP channels are expressed in many tissues including the brain. It is known that KATP channels can affect bursting firing in DA neurons. The previous data in our lab found out that implantation with mini osmotic pumps containing KATP channels opener, diazoxide alleviates LID using 6-OHDA-lesioned mice. We want to know how the KATP channel and DA pathway affect LID and the relationship between KATP channels and DA receptors. The results showed that 6-OHDA-lesion mice implanted with Diazoxide (Diz, KATP channel opener) could alleviate LID but worsen with Glibenclamide (Gbc, KATP channel blocker). Also, the Gbc increases the expression of D3R and Kir6.2, but Diz decreases D3R and Kir6.2 in the striatum. Then we treated pheochromocytoma with stable transfection of human D3R (PC-12/hD3) with D3R agonist. The data showed a higher expression of SUR1 and Kir6.2 than control.

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