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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

排隊等待與消費者反應之研究-以餐廳用餐為例

陳玉潔 Unknown Date (has links)
過去的研究多是以負面的角度去探討等待的現象,的確,等待對許多消費者而言並不是一個良好的經驗,但現實生活中,不乏看到許多人氣商店儘管需要大排長龍,消費者卻還是趨之若鶩,因此本研究欲以餐廳用餐為例,探討排隊等待對消費者態度的影響,本研究主要在了解不同特性的消費者對於排隊是否有不同的反應,在不同的情境下是否也會帶來影響,以及消費者的排隊反應是否會影響到消費者的態度。本文研究架構包含消費者特性和情境因素兩類自變數、中介變數以及消費者態度等三方的相互關係,其中消費者特性包括涉入程度和從眾傾向,中介變數為消費者的排隊反應,包括時間知覺和情緒反應,而消費者的態度包括對需要排隊餐廳認知的價值、對餐廳的滿意度與忠誠度。本研究利用問卷調查和統計分析方法來了解研究變數間的關係。研究結果發現,涉入程度愈高的消費者,雖然等待的情緒反應較負面,但會認為需要排隊的餐廳是有價值的。而在較舒適愉悅的情境下,消費者的時間知覺會較正面,情緒反應會較不負面,這些情境包括用餐時間充裕、用餐前心情愉快等,若情境並非舒適愉悅的,包括像是等待人潮很多、用餐前感到疲累或飢餓,消費者的反應也會較為負面。而對需要排隊餐廳的價值認知與消費者的特性有關,消費者涉入程度愈高或是愈具從眾傾向,消費者愈會認為有價值。而時間知覺和情緒反應會影響消費者的滿意度,滿意度和消費者認知的價值會進而影響忠誠度,消費者的滿意度愈高,或愈是認為需要排隊的餐廳有價值,消費者的忠誠度也會愈高。
2

大腦度巴胺系統在大鼠操作式制約行為中所扮演的角色:以時間為主 / The Role of Brain Dopamine Systems on Operant Conditioned Behavior in the Rat: From Temporal Perspective

鄭瑞光 Unknown Date (has links)
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.

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