本研究以連續性負向對比（successive negative contrast, SNC）動物行為模式進行比較行為所涉及的心理歷程及神經生理系統之探究。實驗首先建立以大白鼠在舔舐不同濃度蔗糖液所引發的連續性負向對比效果之模式，繼而探討飢餓動機在此模式中所扮演的角色，並且以benzodiazepines受體促進劑diazepam進行週邊及中樞注射，期望對此模式之神經行為機制有進一步的發現，並釐清benzodiazepines在當中所扮演的角色。實驗一是為了建立本實驗室大白鼠在舔舐蔗糖液由較高濃度（32﹪）降為較低濃度（4﹪）時產生的連續性負向對比行為的表現，從結果發現剝奪吃食的大白鼠或自由吃食的大白鼠皆有連續性負向對比行為的效果產生，剝奪吃食的大白鼠在減抑負向對比的行為效果比自由吃食的大白鼠還快，而自由吃食的大白鼠在連續性負向對比的行為保持上會持續較久。實驗二是操弄吃食狀態的調換，以檢視大白鼠在負向對比效果表現是否隨飢餓驅力的高低而變化，就結果而言，剝奪吃食改為自由吃食組大白鼠之連續性負向對比行為的產生只發生在蔗糖液濃度變化後的第一、二天，而自由吃食改為剝奪吃食組大白鼠會發生在蔗糖液濃度變化後的四天。實驗三大白鼠進行diazepam腹腔注射，結果發現能有效減抑負向對比效果，但只發生在蔗糖液濃度改變後的第二天。實驗四進行大白鼠腹腔注射diazepam 5 mg/kg以檢視其是否因增加對蔗糖液的喜好因素而減抑了連續性負向對比的效果，結果顯示大白鼠在第一、二天負向對比的效果就不明顯，不過受藥物作用的影響，可以發現舔水次數或舔水量等指標都有增加趨勢，此可解釋為diazepam增加對蔗糖液的喜好得影響。實驗五進行了內側杏仁體及背側海馬體的diazepam微量注射，結果發現蔗糖液濃度改變後第一天，上述兩部位的藥物注射後皆產生負向對比效果，但第二天只有注射內側杏仁體大白鼠減抑了負向對比效果，而背側海馬體大白鼠則繼續保持負向對比效果。綜觀上述結果顯示以舔舐蔗糖液濃度差異所引發連續性負向對比效果所涉及的心理歷程及神經生理系統有其複雜性，benzodiazepines受體促進劑diazepam的藥物測試結果發現會影響此行為模式。 / The present study successive negative contrast (SNC) investigated what psychological processes and neural systems were involved in the comparison behavior. The SNC effect induced by rat’s licking different concentrations of sucrose solution was established and the effect in diazepam (a benzodiazepine agonist) as well as experimental manipulation of food deprivation were observed. In Experiment 1, the SNC effect was induced when the sucrose solution shifted from 32% down to 4%.This effect was observed across the consecutive 4 post-shift days in the free-feeding subjects; however, such effect was gradually diminished in the food-deprived subjects. Experiment 2 manipulated the food deprivation states to study how the hunger drive would affect the SNC. The results revealed that the food-deprived subjects in the pre-shift session show the SNC effect only on the second day of post-shift session with food supplied freely. However, the SNC effects were observed in the consecutive four post-shift days in the subject with free-feeding in the pre-shift session but was then altered into the state of food-deprivation. In Experiment 3, the SNC effect was attenuated by systemic injection of diazepam with the observation of the reduced licking suppression on the second post-shift day. In Experiment 4, with similar manipulation of food supply, diazepam was found to enhance the sucrose licking in addition to its reduction of the SNC effect. The central loci for diazepam to attenuate the SNC effect were investigated in Experiment 5. Although the SNC effect was attenuated by diazepam infused into the medial amygdala or the dorsal hippocampus, the time courses to observe such reduction were different for drug infused into both sites. The study indicates that（a）the SNC effect on licking can be reliably induced by decreasing the sucrose concentration,（b）such effect is attenuated by diazepam via central neural mechanisms. However, further research is needed to determine whether the attenuation of SNC by diazepam is based on the anxiety suppression or appetite enhancement process.

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.