本研究探討舔飲蔗糖液之成本利益情境中，多巴胺受體拮抗劑對舔飲行為配置的影響，以釐清阻斷多巴胺使行為受損的條件與所代表之意義。實驗設計為「高位置高濃度糖液＋低位置低濃度糖液」雙管情境中的舔飲行為，實驗一確立高、低位置分別代表高、低成本後，實驗二至實驗七調整糖液濃度、裝盛容器與舔飲經驗，發現唯有「高位置籠外水管20％糖液＋低位置伸入式水瓶15％糖液」且增加單獨對低瓶的舔飲經驗，方能建立多巴胺受體拮抗劑的「此降彼升」動物模式。實驗八確認「此降彼升」的三要件為低位置是（1）低成本：伸入式容器、（2）高利益：15％糖液、（3）充足經驗：9天舔飲低瓶。實驗九至十一的藥物測試得到前述動物模式可有效區別多巴胺受體拮抗劑、降低食量藥物與干擾動作藥物有不同影響型態。實驗十二發現單管情境與雙管情境的結果有很高的一致性。結論為（1）較低劑量的多巴胺受體拮抗劑並不減少大白鼠對糖液的總需求、不干擾兩者行為間的區辨選擇與轉換能力，（2）舔飲行為不受多巴胺受體拮抗劑干擾的要件為低成本、高利益與充足經驗三者需同時成立，（3）不符三要件之舔飲行為會因多巴胺受體拮抗劑而降低表現量，因此反駁過去認為完結行為不受此類藥物干擾的想法，（4）本研究建立的雙管舔飲情境可有效區分不同藥物作用，值得做為進一步探討多巴胺與行為之間的關係及其神經機制的動物模式。 / This study investigated the effect of dopamine antagonist on licking sucrose solution behavior under cost-benefit condition, which was designed into a 'high-cost high-benefit with low-cost low-benefit' licking test situation. Experiment 1 confirmed that the difference of licking response between high and low positions indicating the cost difference. Experiment 2 to Experiment 7, manipulating the liquid container, sucrose concentration and the experience of licking low position solution, found that rats only increased low position sucrose intake while decreased high position one in 'high tube 20% with low bottle 15% sucrose solution' condition. Experiment 8 further confirmed three factors of low cost, high benefit and plenty experience were necessary for increasing intake of low position in simultaneous contrast to decreasing the intake of high position. Experiment 9 to Experiment 11 evaluated the drug effects of dopamine antagonists, anorectics and motor relaxants on the present animal model. The results showed the different patterns of reaction for these three types of drugs. Experiment 12 revealed the results of single tube condition were consistent with those of cost-benefit condition. Together, these results demonstrated that dopamine antagonist neither decrease the drive for sucrose nor disrupt the abilities to discriminate and select between two tubes under the present model. Three factors of cost, benefit and experience are important to determine dopamine antagonist effect. Therefore, the resistance of consummatory behavior to dopamine dysfunction may be limited for specific situation. And, the cost-benefit licking model can be useful for further investigation of neurobehavioral mechanism of dopamine system.

過去有關壓力的研究指出，當對實驗動物施予單次禁錮、足部或尾部電擊或是實驗者的抓取動作等壓力源時，其大腦中的前額葉皮質、杏仁核、依核或是紋狀體等處會有隨壓力源產生的多巴胺分泌量增加現象。相對於壓力源對腦中神經化學物質的探討，壓力源對與學習制約有關的行為影響的相關研究證據迄今如缺，因此本研究企圖建立單次壓力源操弄對場地制約偏好行為的動物模式。實驗一A對大白鼠施予單次30分鐘的高台壓力源，發現確實可建立場地制約偏好行為。實驗一B操弄單次高台壓力源觀察其對實驗動物自發性活動量的影響，結果發現其對於實驗受試在大動作持續時問上具有抑制效果。實驗一C操弄單次高台壓力源後的0、30、60及120分鐘時採取實驗受試的前額葉皮質、海馬體、杏仁核、依核及紋狀體等五處組織，檢驗其多巴胺、血清張力素及代謝物的含量。結果發現除海馬體外的四個部位的多巴胺量及其代謝物分別在不同採集時間點有不等的顯著增加現象。血清張力素的變化量在各個部位不及多巴胺。實驗二及實驗三分別經由周邊或中樞前額葉皮質微量注射多巴胺D₁與D₂專屬受體拮抗劑，結果發現其可抑制曲單次高台壓力源操弄所建立的場地制約偏好行為。綜合上述結果，單次高台壓力源的操弄確實可引發大白鼠大腦中的多巴胺量增加藉以形成場地制約偏好行為，而此場地制約偏好行為所依賴的多巴腰量增加位置推論其是依核而非前額葉皮質。另外，多巴胺D1與D2受體對此高台壓力源引發的場地制約偏好行為所扮演的角色相當。 / When experimental animals under single stressor, such as restraint, foot, or tail-shock, or handing, an immediate and robust releasing of dopamine appears in the prefrontal cortex, amygdala, nucleus accumbens, or striatum. In contrast to these neurochemical findings, the behavioral effects under stress are rarely studied and remained uncertain. The purpose of this study was to establish an animal model of single stress-induced conditioned place preference (CPP). Experiment 1A found that the CPP can be induced by a single high-plate stressor. Experiment 1B investigated the effects of this single high plate stressor on rats' locomotion, this stressor was found to inhibit the large movement as measured by duration. Experiment 1C investigated the timing course of this stressor on dopamine, serotonin, and their metabolities in the prefrontal cortex, hippocampus, amygdala, nucleus accumbens, and striatum. The results showed that all the areas, except hippocampus, had distinct patterns of changes on dopamine, serotonin and their metabolities at different times' after stress. Experiment 2 and 3, examined the effects ofdopamine D1 or D2 receptor antagonists, administered respectively via intraperitoneal or local infusion into the prefrontal cortex, on the CPP formed after high-plate stress. The results showed that these drug manipulations can inhibit stress-induced CPP. Taken together, these results indicated the CPP formed after high-plate stressor is developed on the immediate increase ofdopamine releases in the nucleus accumbens and prefrontal cortex. These neurochemical alterations are more profound in the nucleus accumbens than the prefrontal cortex. However, the dopamine D₁ and D₂ receptor in the prefrontal cortex are also important for the formation of CPP after high-plate stressor.