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.

自2005年以降，我國針對是否開放含萊克多巴胺畜產品進口之問題即屬多事之秋，其主因係在食品添加物專家委員會（Joint FAO/WHO Expert Committee on Food Additives，簡稱JECFA）所擬每日容許攝食量下，國際上之相關科學研究無法確切證明萊克多巴胺是否完全安全，抑或其可能對於人體造成之危害及程度，因此多數肉品出口國仍常於家畜飼養過程中添加萊克多巴胺於飼料中，藉以增加畜產品之瘦肉比例並提升經濟效率；另一方面，由於不肖業者違法使用乙型受體素（如克崙特羅、沙丁胺醇）導致人體中毒的案件時有所聞，影響民眾對於畜產品的消費意願及產業發展，是故雖然萊克多巴胺之毒性相較於其他乙型受體素為低，惟受他種毒素高出數倍的乙型受體素之累，在我國自2006年起亦屬禁用之列。在國際食品標準委員會（Codex Alimentarius Commission，簡稱Codex委員會）於去（2012）年以普通多數決之方式制定萊克多巴胺的國際標準後，我國遂修訂食品衛生管理法第11條（2013年新法第15條）、第17-1條 （新法第25條）及動物用藥殘留標準第3條，並公告農防字第1011473960號之行政命令，採行「安全容許、牛豬分離、強制標示、排除內臟」之檢疫政策，在牛肉（含脂肪）的部分採行與國際標準相同之檢疫標準；惟在豬肉及內臟的部分，則為兼顧「國人特殊膳食習慣」及「相關產業發展」，仍維持既有「零檢出」的檢疫政策，全面禁止含萊克多巴胺的畜產品進口。針對此我國特殊之管制作法，本文將以國際經貿法的觀點，依據WTO協定中與檢疫措施最密切相關的SPS協定規範、過往案例之判決及相關文獻，分析我國進口檢疫規定之適法性，藉以思考目前畜產品進口的議題，並判斷該措施將來是否存在遭非難之可能，希冀能對於我國日後檢疫政策走向提供一實質性之參考及展望。 / Since 2005, the issue of liberalizing the import of meat containing Ractopamine had sparked great controversy in Taiwan, resulting from the lack of clear and definite scientific evidences worldwide to prove the harmlessness toward human body under JECFA’s maximal residue level and acceptable daily intake. Owing to the abusing of other much more poisonous Beta-adrenergic agonist (e.g., Clenbuterol, Salbutamol) by some of illegal stockbreeders causing the vibration of meat market and industry, Taiwan’s government had decided to ban the residual of Beta-adrenergic agonist including Ractopamine contained in both domestic and import meat products since 2006. After Codex Alimentarius Commission finally voted through the international standard of Ractopamine in 2012, Taiwan’s Legislative Yuan amended former regulations, approving the import of beef which conformed to Codex’s international standard, while still remained the prohibition of pork containing Ractopamine. This essay staying with the view of international trade law, in particular the Agreement on the Application of Sanitary and Phytosanitary Measures under World Trade Organization, tries to analyze the consistency of Taiwan’s meat regulations with the SPS agreement in order to prospect Taiwan’s trade policy and meat regulations regarding Ractopamine in the future.

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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.

雖然焦慮是一種普遍存在之情感性心智活動，迄今仍無充份解釋之實證資料。本研究主要是利用一種焦慮症相關的動物模式，即抬高式T形迷津，探討與焦慮症有關的神經行為機制。整部研究分兩大實驗，分別探討抬高式T形迷津的行為建構動力與破壞依核次級區域在抬高式T形迷津或其他焦慮作業上之行為表現。在實驗一檢驗抬高式T形迷津的行為內涵方面，共有四個實驗：實驗一A探討抬高式T形迷津抑制性躲避行為是否呈現消除現象；實驗一B探討破壞制約害怕神經網路對抬高式T形迷津之抑制性躲避行為的影響，並檢測自發性運動量的改變是否造成干擾效果；實驗一C探討事前暴露經驗對脫逃行為的意義；實驗一D檢測脫逃及抑制性躲避實驗程序互相干擾之可能性。實驗二探討可能涉及抬高式T形迷津或其他焦慮作業的神經機制，針對破壞依核次級區域對焦慮行為的影響進行檢測。此部分包含三個實驗，實驗二A探討依核次級區域受損對傳統焦慮動物模式抬高式十字迷津行為的影響；實驗二B採用已在實驗一建立行為效度的抬高式T形迷津，檢驗破壞依核次級區域後的迷津行為表現，並檢驗依核次級區域受損是否影響受試自發性運動量變化，以致干擾抬高式T形迷津的行為表現。另為深入探討依核的功能角色，實驗二C利用其他嫌惡作業測試破壞依核次級區域對制約躲避電擊行為的影響。實驗一結果顯示抑制性躲避行為是一包含制約害怕及探索行為等多重歷程的行為模式，而脫逃行為對情緒狀態的改變不敏感，且易受抑制性躲避作業的影響。實驗二發現破壞依核殼區同時減抑受試在抬高式十字迷津的危機評估行為、抬高式T形迷津之抑制性躲避行為及制約躲避電擊行為；而破壞依核核區的減抑效果僅見於抬高式T形迷津與制約躲避電擊作業。三個嫌惡作業的結果顯示依核核區與殼區皆涉及制約害怕歷程，但兩區的受損會表現不同焦慮行為，並在抬高式十字迷津之危機評估行為中表現出來。綜合上述二大部分實驗結果，本研究對抬高式T形迷津的行為內涵有更進一步的瞭解，並特別藉依核次級區域破壞的行為測試資料，推估中腦多巴胺系統與傳統理論所指邊緣系統在實證性解釋焦慮具同樣關鍵角色。 / Although anxiety is a well-recognized affective mental reaction, its phenomenon is not fully characterized by the empirical data. By employing a recently developed animal model named the elevated T maze (ETM), the present study investigated the neurobehavioral mechanisms of anxiety. There were two major parts of experiments designed to respectively examine the validity of this task and the involvement of limbic related areas on anxious behavior. Regarding the first part of experiments, Experiment 1A examined the effects of extinction on the inhibitory avoidance of ETM; Experiment 1B evaluated the lesions of six limbic related areas on the measures of inhibitory avoidance and escape; Experiment 1C investigated how pre-exposure experience of stress would affect the ETM behavior; Experiment 1D tested the potential affectiveness derived from different sequences of the test procedure on EMT. The second part of experiments mainly focused on comparing the lesion effects of nucleus accumbens subareas (core and shell) on behavioral measures from three anxiety-related tasks. Elevated plus maze, ETM, and active avoidance were adopted respectively in the experiments of 2A, 2B, and 2C. Results of the first part of experiments indicated 1) inhibitory avoidance of ETM containing fear conditioning and exploration components, and 2) less sensitivity to experimental manipulation for the escape of ETM. In the second part of experiments, the shell lesion significant attenuated the risk assessment behavior of elevated plus maze and inhibitory avoidance of ETM and active avoidance tasks, whereas the core lesion only produced the latter part of impairment. Both core and shell subareas are thus inferred to be involved in the conditioned avoidance, and lesions of these two areas may exert different patterns of anxious behavior. Together, the present study further characterized behavioral components of ETM. With a more systemic work in comparing lesion data of nucleus accumbens over three anxiety-related tasks, it is then suggested that the midbrain dopamine system is as crucial as the traditionally-known limbic system the traditional in terms of providing empirical explanation for the anxiety.

「風險決策」行為非常普遍的存在於吾人之日常生活中，而選項所帶來的風險和獎勵是吾人進行決策時的重要考量因素。風險選擇的適當與否，對於個體的生存扮演著相當重要的角色。在以往的文獻中，對於決策的行為歷程已有所關注及探討，但對於風險選擇行為的神經生理機制迄今未明。本研究藉由大白鼠於T字迷津中，選擇確定之低酬賞或高不確定性之高酬賞的行為表現，進行風險選擇行為的探討。本研究中以兩項主要實驗，探討風險選擇行為之神經行為機制。實驗1a中，確定之低酬賞端固定呈現1顆食物粒，而高不確定性之高酬賞端則同時操弄酬賞物機率(50%、25%及12.5%)以及酬賞物的量(2、4及8顆)，以系統性地檢驗期望值(0.5、1和2)於此風險選擇行為中扮演的角色。行為結果顯示當風險較低時，大白鼠會選擇高不確定性之高酬賞端；而風險較高時，則轉為選擇確定之低酬賞端。實驗1b中，系統性地施打不同劑量之安非他命，探討多巴胺系統在此風險選擇行為中之機制。實驗結果顯示施打安非他命後，大白鼠表現出相對地追求風險之行為，亦即選擇高不確定之高酬賞端之比例顯著高於控制組。實驗2中，藉由毀除大腦特定部位(依核、背外側之紋狀體、眶前額皮質、內側之前額皮質)，檢驗風險選擇行為之神經基礎。毀除後之結果顯示，僅有依核受到毀除之大白鼠表現出相對地趨避風險之選擇行為。綜合以上結果，本研究建立之風險選擇行為與多巴胺有關，而依核在此行為歷程中扮演重要的調節角色。 / Many decisions people make every day involve uncertainty where both risks and rewards associated with each option need to be considered. Behavioral performance associated to risk-based choice appears wildly over the lifespan, and the fitness of risky choice behavior plays an important role in individual survival. Despite a growing body of research has focused to investigate the neurobiology of decision making, little is known about the neurobehavioral mechanisms of risky choice behavior. Based on a pilot work, this study used a T-maze to study decision under a probability-based risk in the rat. The subject was assessed on making choice to obtain either a large reward associated with risk of non-reward “empty” or a small reward ensured for every entry. Two experiments were conducted in this project to investigate neurobehavioral mechanisms of probabilistic risky choice behavior. In Experiment 1a, probabilistic risky choice behavior was systemically assessed under three expected values (0.5, 1.0, and 2.0) by manipulating the probabilities of reward presence (50%, 25%, and 12.5%) and the reward magnitude (2, 4, or 8 pellets) in the probabilistic high reward (PHR) arm. Behavioral data showed that the subject chose the probabilistic high reward in a lower risk condition but would shift to the choice of certain low reward (CLR) as the risk is increased. In Experiment 1b, the dose effects of amphetamine on this probabilistic risky choice task was tested to verify whether the dopaminergic mechanism was involved. Amphetamine, presumably activating brain dopamine systems, produced a relatively risk-seeking effect on the present behavioral task. In Experiment 2, the excitoneurotoxic lesion was conducted in the nucleus accumbens, the dorsolateral striatum, the orbitofrontal cortex, and the medial prefrontal cortex to examine the neural substrates for this probabilistic risky choice behavior. The results showed that the lesion of the nucleus accumbens significantly produced a relatively risk-averse effect on the present behavioral task, as compared to the lesions made on the other three brain areas. In conclusion, the probabilistic risky choice behavior established in the present study is dopamine dependent. And, the nucleus accumbens plays a major role of mediating this behavioral processing.

蛋白激酶CK2（Casine kinase 2）為四單體所構成，針對配受質蛋白之絲胺酸或蘇胺酸位置進行磷酸化，先前研究已經發現在紋狀體腦區之CK2的表現量與活性皆高於大腦中其餘腦區，而紋狀體腦區主要神經細胞為-氨基丁酸神經元（GABAergic neurons）的medium spiny neuron（MSN），會受到來自黑質多巴胺神經細胞（dopaminergic neurons）的調控。此外，DARPP-32（dopamine- and cAMP-regulated phosphoprotein, Mr 32 kDA）蛋白亦被發現大量表現於在MSN細胞中，且為CK2之受質蛋白質。雖然CK2已被證實參與多巴胺神經元的神經保護機制，但是否參與MSN細胞對運動行為調控之生理機制仍未清楚。由於已有研究發現施予1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）藥物處理造成黑質-紋狀體腦區受損之老鼠腦內-氨基丁酸（GABA）的生合成酵素─麩胺酸脫羧酵素67（GAD67）表現量與正常老鼠不同，因此本論文研究的主題擬在大鼠實驗模式中利用MPP+造成投射至紋狀體之多巴胺神經細胞受損，探討當多巴胺調控紋狀體神經細胞能力缺失的狀態下，MSN細胞之CK2、DARPP-32和GAD蛋白表現與動物運動行為之相關性。 實驗結果發現，直接於紋狀體給予1-甲基-4-苯基碘化啶 （MPP+ Iodide）皆會造成CK2、DARPP-32以及GAD67之蛋白質含量的減少，多巴胺及其代謝物和GABA等神經化學傳遞物質亦有減少的現象；另外，在MPP+給予前分別操弄CK2或DARPP-32 胺基酸Ser102磷酸化的表現，皆會改變GAD67蛋白質含量與黑質酪胺酸羥化酶（Tyrosine Hydroxylase, TH）蛋白質含量，同時神經化學傳遞物質的含量或代謝亦有改變。由現有之結果推測CK2/DARPP-32/GAD67細胞訊息傳遞機制可能參與巴金森氏症運動行為失常之細胞層面的調控。 / Protein kinase CK2 is a heterotetrameric and serine/threonine protein kinase. Its protein levels and activity are found to be elevated in the striatum when compared to other brain areas. CK2 is known to involve in the neuroprotective effects of dopaminergic neurons, whether it also regulates the neuronal function relative to motor behaviors is still unclear. DARPP-32 protein is known as one of the substrates for CK2 and is highly expressed in the GABAergic medium spiny neurons (MSN) responsible for dopamine stimulation in the striatum. Furthermore, other studies have indicated that the expression of glutamic acid decarboxylase 67 (GAD67) mRNA and protein was different in the striatum of MPTP vs. naïve animals, which is one of the enzymes responsible for the synthesis of neurotransmitter GABA. In the present study, we observed that the parallel changes in protein levels of CK2, DARPP-32 and GAD67 in the striatum and TH in the substantia nigra of MPP+-treated. We also found that manipulation of CK2 or DARPP-32 gene expression aggravated the MPP+-induced neuropathological dificts. The present results suggest that CK2/DARPP-32/GAD67 signaling pathway might involve in the cellular mechanism of motor-deficit in Parkinson’s disease.

透過神經科學的研究，對於大腦的行為功能已有一定的認識，不同於以往的認識，目前認為神經行為機制不只由單一腦區或單一神經化學系統所調控。深部大腦電刺激經常被用來研究特定腦區的行為功能。但是，深部大腦電刺激的作用機制仍然不清楚。最近幾年臨床研究發現，利用電刺激在側韁核成功的治療憂鬱症患者。然而，目前認為側韁核與多巴胺系統互為負回饋作用，共同參與在動機行為的酬賞反應中。本實驗室先前的研究顯示，破壞韁核造成區辨性低頻操作式制約行為 (簡稱DRL行為)學習的障礙，然而，電刺激在側韁核造成DRL行為表現的結果還是未知的。所以，本實驗主要以電刺激在側韁核觀察大鼠行為上的改變，探討側韁核在行為上參與的功能。實驗一的結果顯示電刺激在側韁核並不影響自發性運動能力，在不同電流強度的刺激下也不會影響。實驗二的結果顯示電刺激在側韁核造成DRL 15秒的行為有類安非他命效果之行為表現，在高頻率電刺激有較顯著類安非他命的效果。實驗三的結果顯示電刺激在側韁核造成DRL 15秒的行為之影響，會被多巴胺受體抑制劑所抵消，而單獨注射巴胺受體抑制劑並不影響DRL 15秒的行為。實驗四的結果顯示電刺激在側韁核造成DRL 15秒的行為之影響，不會被正腎上腺素受體抑制劑所抵消。實驗五的結果顯示電刺激在側韁核造成DRL 72秒的行為之影響並不如DRL 15秒的行為顯著。實驗六的結果顯示電刺激在側韁核並不會造成大鼠無法區辨酬賞的量。綜合而言，側韁核在動機行為的角色，是透過影響多巴胺系統造成行為的改變。 / Behavioral function of the brain has been studied in neuroscience and progressively accumulated informative data to reveal the neurobehavioral mechanisms. It is now realized that those underlying mechanisms of behaviors is not as such simple as previous thought of limiting only in one locus of the brain or solely by one neurochemical system. The deep brain stimulation is usually used to study the behavioral function of specific brain regions. However, the mechanism of the deep brain stimulation is still unclear. The previous study has shown that electrical stimulation of the lateral habenula (LHb) successfully treated depression symptoms in the patients. It is proposed that an inhibitory role of LHb on the mibrain dopamine (DA) system which mediates the reward-related behavior. A previous study of this lab showed that lesion of habenula impaired the acquisition of differential reinforcement of low-rate responding (DRL) behavior. But, the effect of LHb stimulation on the DRL behavior is still unclear. To determine the functions of LHb involving in the behavior, the electrical stimulation was applied in LHb to observe the behavioral change of rats. The results of Experiment 1 showed that the LHb stimulation had no effect on locomotor activity. In Experiment 2, the LHb stimulation was shown to affect DRL 15-s behavior, which effects were similar to those affected by amphetamine. Experiment 3 showed that the DA receptor antagonists reversed the effects of LHb stimulation, while experiment 4 showed that norepinephrine (NE) receptor antagonists had no reversal effect on DRL 15-s behavior. In Experiment 5, the amphetamine-like behavior induced by LHb stimulation had subtle effects on DRL 72-s behavior. Experiment 6 showed that the LHb stimulation had no effect on a discrimination task. These data suggest that the LHb modulating DRL behavior is DA-dependent.

周邊注射安非它命能夠影響動物受試在表現與時間知覺有關的操作式制約行為作業，歷來被研究者認為是大腦多巴胺神經系統與動物時間知覺系統有關的主要證據之一。本研究所共同採用的研究方法為先注射多巴胺受體專屬拮抗劑再於大鼠受試周邊腹腔注射安非它命的方式探討安非它命影響大鼠時間知覺的大腦機制為何。實驗一利用區辨性增強低頻反應作業觀察周邊注射多巴胺受體專屬拮抗劑何者可以反制周邊安非它命對此作業的影響效果，結果發現多巴胺D1受體拮抗劑SCH23390與D2受體拮抗劑raclopride均可反制周邊安非它命的效果。實驗二同樣利用區辨性增強低頻反應作業，但是將SCH23390與raclopride分別注入海馬迴、背側中區紋狀體、腹側側邊紋狀體、依核、內側前額葉皮質以及腹側頂蓋區等六個部位，觀察何種多巴胺受體拮抗劑可在那些大腦部位產生反制周邊安非它命的效果。結果發現SCH23390可在海馬迴、依核、內側前額葉皮質以及腹側頂蓋區等四個部位產生反制周邊安非它命的效果，而raclopride可在腹側側邊紋狀體與內側前額葉皮質兩個部位產生同樣的反制效果。實驗三利用高峰時距作業觀察SCH23390在海馬迴與內側前額葉皮質是否能反制周邊安非它命對此作業的影響效果，結果發現SCH23390僅在海馬迴會影響大鼠受試的正常表現，特別是在與周邊安非它命同時注射的時候。綜合以上結果顯示，周邊注射安非它命能夠使大鼠受試在區辨性增強低頻反應作業當中表現出時間知覺變快的傾向，這個效果需要同時透過大腦內的海馬迴、依核、內側前額葉皮質以及腹側頂蓋區的多巴胺D1類受體和腹側側邊紋狀體與內側前額葉皮質的多巴胺D2類受體。 / The central dopaminergic system has been hypothesized to play a role in time perception based on the results that peripheral injections of d-amphetamine alter the responses in time-related operant conditioned behavioral tasks. The present study investigated the effect by injecting specific dopamine receptor antagonists before peripheral d-amphetamine injections in rats. Data from Experiment I showed that both peripheral the dopamine receptor D1 antagonist SCH23390 and D2 antagonist raclopride could attenuate the response alteration on differential reinforcement of low-rates responding task induced by peripheral d-amphetamine. By using the DRL task, Experiment 2 employed the microjeciton technique to determine the neural substrates for the DA receptor antagonist to attenuate the effect of peripheral d-amphetamine. The infusion sites for DA receptor antagonist were the hippocampus, the dorsomedial striatum, the ventrolateral striatum, the nucleus accumbens, the medial prefrontal cortex, and the ventral tegme ntal area. The results showed that SCH23390 infused into the hippocampus, the nucleus accumbens, the medial prefrontal cortex, the ventral tegmental area could attenuate the effect induced by peripheral d-amphetamine, and such attenuation effects were also observed for raclopride infused into the ventrolateral striatum, the medial prefrontal cortex. Experiment 3 tried to confirm the results of Experiment 2 by microinjecting SCH23390 in hippocampus and medial prefrontal cortex under peak-interval task. Only SCH23390 in the hippocampus altered the subject's normal performance in this task especially when combined with peripheral injection of d-amphetamine. In conclusion, that the response alteration on the DRL task induced by peripheral injection ofd-amphetamine suggests the subject's timing perception being accelerated. These effects of d-amphetamine were mediated by simultaneous activation of multiple dopamine receptor subtypes including D1 receptors located in the hippocampus, nucleus accumbens, medial pref rontal cortex, ventral tegmental area, as well as D2 receptors located in the ventrolateral striatum, medial prefrontal cortex.