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題名:Haloperidol干擾正向與負向味覺刺激的反應:多巴胺阻斷劑的"Anhedonia"假設之檢視
作者:黃智偉
作者(外文):Andrew Chih Wei Huang
校院名稱:國立中正大學
系所名稱:心理學研究所
指導教授:蕭世朗
學位類別:博士
出版日期:2003
主題關鍵詞:多巴胺負向與正向酬償刺激顯著性酬償效果中央杏仁核基側邊杏仁核dopamineaversion and rewardsalient stimulireinforcementcentral amygdalabasolateral amygdala
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本研究使用味覺嫌惡制約及味覺溶液攝食的動物行為模式,檢驗腦內多巴胺系統是否牽涉正向及負向未制約刺激的酬償效果。結果顯示: (a)多巴胺阻斷劑haloperidol注射於未制約刺激前分別能削弱正向刺激安非他命及負向刺激氯化鋰引發的味覺嫌惡制約,但投藥於未制約刺激之後並無產生此削弱效果,且haloperidol本身與糖精液配對不會產生味覺嫌惡制約,表示haloperidol 很可能阻斷的是未制約刺激且無論此刺激的價值特性。(b)在haloperidol不影響動作系統的低劑量注射下,低濃度的正向味覺刺激糖水的攝取量減低而等張的負向味覺刺激氯化鋰攝取量增加,其他味覺溶液(苦味的高低濃度奎寧,鹹味的等張食鹽水,及高濃度的糖水)的攝取量不受影響。(c)等張食鹽水在配對氯化鋰後會產生味覺嫌惡制約,但此效果不受haloperidol的影響。(d) Haloperidol注射於腦內中央或基側邊杏仁核區,不會影響等張食鹽水、正向糖水及負向氯化鋰水溶液的攝食。
表示腦內多巴胺系統不僅牽涉正向未制約刺激也影響負向未制約刺激,此結果修正早期多巴胺anhedonia 的假設,支持最近的腦內多巴胺系統牽涉刺激顯著性的新假設。研究結果並對該假設提出更進一步的釐清,認為所謂的刺激顯著性很可能指的不是刺激的新奇性(novelty),而是刺激的酬賞價值(reinforcing value),而腦內多巴胺系統可能負責此一功能。然而本研究中制約學習後的食鹽水降低的攝取量為何不被haloperidol阻斷,而杏仁核內haloperidol的微量注射為何無法影響正向糖水及負向氯化鋰味覺溶液的攝食,這些仍待解決的問題成為後續研究的基礎。
許多關於腦內多巴胺系統功能的新問題及新議題在本研究發現,仍待後續的研究釐清。
The present study examined the influence of a nonselective D2 receptor antagonist, haloperidol, on attenuating the effect of rewarding and aversive stimuli in the conditioned taste aversion and the innate gustatory solution intake paradigms. The results showed that (a) haloperidol attenuated the reduction of saccharin intake induced by the rewarding US agent amphetamine or aversive US agent LiCl no matter what a valence of them when haloperidol was given prior to (but not posterior to) the US. Besides, haloperidol by itself did not generate the suppression of saccharin intake during the conditioning sessions. (b) The low dose of 0.1 mg/kg haloperidol, which did not affect licking responses of water intake, attenuated the reinforcing effect of rewarding sucrose and aversive LiCl. It appeared to reduce the intake of low concentration of sucrose on the drug session and increase the amount of NaCl intake on the testing session. However, this effect did not occur under the low and high concentrations of quinine, isotonic NaCl, and the high concentration of sucrose solutions. (c) After conditioning with an aversive agent LiCl, NaCl induced a conditioned suppression. However, this effect was not blocked by the pretreatment of haloperidol. (d) Haloperidol respectively infused into the central amygdaloid nucleus and the basolateral amygdaloid nuclei did not affect the reinforcing potency of rewarding sucrose and aversive LiCl solutions.
Thus, the brain DA system mediated the impact of both aversive or rewarding US. The findings revise the anhedonia hypothesis of DA blocking and support the saliency hypothesis of the brain DA system. However, these data indicated that the saliency of a stimulus is not conferred by the novelty of stimuli. Rather, it is probably bestowed by the reinforcing value of stimuli. Taken together, the brain DA system probably plays a crucial role in representing the reinforcing potency of stimuli. However, whether a stimulus possesses reinforcing value seems to depend on the animals’ condition, except few primary reinforcers. The results of this thesis research raise new issues that require further investigation in the future.
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