藥物成癮－－由腦神經化學看求藥行為   全文下載

Drug Addiction-the Neurochemical Perspective of Brain in Drug-Seeking Behavior

藥物成癮之神經生物學機制的根本探尋在於：個體如何從偶而隨興的使用，轉成為難以自我克制的藥物渴望，和容易再發求藥行為的長期成癮狀態。反覆使用精神刺激劑可造成實驗動物出現行為致敏化。研究指出致敏化在中腦──邊緣及中腦──皮質神經路徑所引起的神經調適，與個體對成癮藥物的求藥行為之增強有密切關連。而與致敏化有關的神經傳導物質，最主要有多巴胺與麩胺酸。本文回顧相關文獻，重點以安非他命類與古柯鹼藥物的報告分析，說明在中腦邊緣、皮質神經迴路的神經傳導物質在致敏化的轉變，以及其與成癮藥物的求藥行為的重要觀念和研究發現。而近年來對於透過關聯學習機制，在經常接受藥物的環境與激發長期用藥者之求藥行為的關係，也頗受注意，文中也一併介紹。

A critical challenge of the investigation in the neurobiological mechanism of drug addiction is how acute actions become transformed into chronic effects that underlie the compulsive drug-seeking and craving in addiction. Repeated administrations of psychostimulants can enhance the behavioral response upon reinstatement of the drug, a prominent phenomenon known as behavioral sensitization. It has been implicated that the neuronal changes brought about by sensitization in the mesocorticolimbic pathways have close relationship with compulsive drug seeking in addicts. Dopamine and glutamate are the two major neurotransmitters involved in the sensitization of abused drugs. The authors reviewed literature pertinent to amphetamine and cocaine addiction in order to address the recent important concepts and findings in dopaminergic and glutamatergic neurochemical systems of mesolimbic and mesocortical circuits associated with drug-related behavior. The present review also discusses the role of associative learning as manifested in the relationship between environmental cues of drug administration and intractable drug-seeking behavior. 藥物成癮之神經生物學機制的根本探尋在於：個體如何從偶而隨興的使用，轉成為難以自我克制的藥物渴望，和容易再發求藥行為的長期成癮狀態。反覆使用精神刺激劑可造成實驗動物出現行為致敏化。研究指出致敏化在中腦──邊緣及中腦──皮質神經路徑所引起的神經調適，與個體對成癮藥物的求藥行為之增強有密切關連。而與致敏化有關的神經傳導物質，最主要有多巴胺與麩胺酸。本文回顧相關文獻，重點以安非他命類與古柯鹼藥物的報告分析，說明在中腦邊緣、皮質神經迴路的神經傳導物質在致敏化的轉變，以及其與成癮藥物的求藥行為的重要觀念和研究發現。而近年來對於透過關聯學習機制，在經常接受藥物的環境與激發長期用藥者之求藥行為的關係，也頗受注意，文中也一併介紹。