過去化學突觸(chemical synapse)特性的改變一直被認為是造成生物神經系統可塑性的主要原因，然而，近幾年來有許多的研究者發現神經傳導物質(neurotransmitter)可能造成電突觸(electrical synapse)在神經傳導特性上的改變，這種改變可能也是造成神經可塑性的另一種原因。2000年Alves 等人所發表的一篇文章提供了一些有關這方面的研究與討論。如文獻探討所示，目前已發現許多由化學突觸(chemical synapse)所釋放的神經傳遞物，其中包含穀氨酸(glutamate)、5-羥色胺(serotonin，簡寫5-HT)、多巴胺(dopamine)以及乙醯膽鹼(Acetylcholine，簡寫ACh)會造成電突觸特性的改變。然而整體而言，此領域的研究迄今仍相對少見。
因此本研究的主要目的在於提供一個螯蝦逃跑神經迴路中的神經傳導物質—乙醯膽鹼可能造成電突觸神經傳導特性改變的證據，並為此提出適當的解釋。研究方法為電生理技術和藥理法，其中包括在突觸前神經細胞內打入小電流並在與其藉由電突觸相連的突觸後神經細胞記錄其反應。另外，乙醯膽鹼及其興奮劑和詰抗劑來觀察電突觸神經傳導特性是否受到改變。研究結果的數據分析方法包括統計分析(平均值、標準差以及線性迴歸)和曲線擬合(最小平方法)。
研究結果顯示當乙醯膽鹼的其中一種感受器—毒蕈膽鹼類乙醯膽鹼感受器—的興奮劑被加入正在記錄的神經細胞的緩衝液以後，會造成連接前後細胞的電突觸的神經傳導訊號變大。然而，加入乙醯膽鹼的另一種感受器—尼古丁乙醯膽鹼感受器的興奮劑則造成電突觸的神經傳導訊號減少。此外，加入乙醯膽鹼並不會造成電突觸的神經傳導訊號明顯的增加或減少，然而，若先在緩衝液中加入尼古丁乙醯膽鹼感受器的詰抗劑，然後再加入乙醯膽鹼則會造成電突觸的神經傳導訊號明顯增加。因此，我們推測在螯蝦逃跑神經迴路中，乙醯膽鹼透過nAChR 對LG產生抑制作用，但會透過mAChR對LG產生增強作用。
所以，此研究除了希望能解釋毒蕈膽鹼類乙醯膽鹼感受器和尼古丁乙醯膽鹼感受器是如何在螯蝦逃跑的神經迴路中扮演的角色，也可藉此進一步了解乙醯膽鹼是如何改變電突觸的神經傳導特性。

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