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研究生:張雅惠
研究生(外文):Chang, Yea Heuy
論文名稱:麩胺酸對心理興奮劑引發制約性場地偏好行為之探討
論文名稱(外文):The effects of glutamate on psychostimulant induced conditioned place preference
指導教授:廖瑞銘廖瑞銘引用關係
指導教授(外文):Ray Ming Liao
學位類別:碩士
校院名稱:國立政治大學
系所名稱:心理學系
學門:社會及行為科學學門
學類:心理學類
論文種類:學術論文
論文出版年:1998
畢業學年度:86
語文別:中文
論文頁數:71
中文關鍵詞:制約性場地偏好古柯鹼阿控博核安非他命麩胺酸
外文關鍵詞:cppcocaineaccumbensAMPHETAMINEGLUTAMATE
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安非他命與古柯鹼皆屬心理興奮性藥物(psychostimulants),在藥理上
有很多功能相似的機制,而且兩種藥物濫用成癮的問題一直是臨床及基礎
研究所關心的問題。就動物行為模式而言,安非他命與古柯鹼具有影響包
括反射性及制約學習性的行為表現的效果。若針對藥物的酬賞性做探討時
,制約性場地偏好行為模式的相關研究益發受到重視,本研究實驗一先針
對此作業之操弄時間及環境變項做一探討,再研究安非他命與古柯鹼之作
用機制。過去的研究發現,週邊注射安非他命或古柯鹼與某環境刺激配對
能引發制約性引發場地偏好的傾向,但兩藥的行為現象卻對藥理的操弄呈
不一致的結果,隱含兩藥背後的神經機制可能也不同。其中阿控博核是一
個值得再驗證的區域。阿控博核被認為是動機系統與運動系統的介面。此
部位因其解剖及生化功能的異質性,故實驗二針對其次分區進行中樞藥物
注射,於是直接將安非他命(10,15μg)與古柯鹼(50,100μg)分別注射
於阿控博核之次級區。結果發現安非他命直接注入阿控博核核區或古柯鹼
注入阿控博核殼區可表現顯著的場地偏好效果。基於阿控博核所含有的麩
胺酸神經末梢源自內側前額葉皮質,實驗三則發現安非他命或古柯鹼注入
內側前額葉皮質可引發制約性場地偏好行為。實驗四將麩胺酸專屬受體抑
制劑與安非他命共同注入核區或與古柯鹼共同注入殼區,結果發現不論
NMDA或non-NMDA受體抑制劑均減抑了安非他命與古柯鹼注入阿控博核不同
區所引發之制約性場地偏好的效果。最後實驗五利用內側前額葉遭破壞的
受試,發現古柯鹼注入阿控博核殼區所引發之制約性場地偏好的效果受損
,但不影響安非他命注入阿控博核核區所引發之制約性場地偏好的效果。
綜觀上述結果顯示安非他命與古柯鹼的酬賞特質所引發行為的神經機制可
能不同,腦中之內側前額葉皮質及阿控博核對兩藥的行為效果有不同的涉
入。
The function of the nucleus accumbens (NACC) has been
suggestedto play an important role of the rewarding effects of
psychostimulants.It is hypothesized that the neural substrates
for amphetamine and cocaineto produce behavioral effects can be
different. As conducted in Experiment 1, a conditioned place
preference (CPP) task with procedures for amphetamine
microinjection was established from the manipulation of
conditioning environment. In considering the heterogeneity of
NACC, Experiments 2 investigated the potentiality of the CPP
effects after local infusion of amphetamine (10, 15 μg/site) or
cocaine (50, 100 μg/site) into the core and shell subareas of
NACC. Amphetamine microinjection into the NACC core
significantly produced CPP, whereas such effect only appeared
under treatment of the high dose of cocaine into the shell area.
Lack of the CPP effects for amphetamine or cocaine infused into
the boundary areas of the core and shell regions was seen in
Experiment 2 (part B). In Experiment 3, the involvement of the
medial prefrontal cortex (mPFC) was challenged for amphetamine
and cocaine on the CPP task. Both doses of cocaine and the low
dose of amphetamine locally infused in mPFC significantly
produced CPP. In Experiment 4, glutamatergic NMDA receptor
antagonist APV (0.5, 1 μg/site) and non-NMDA receptor
antagonist CNQX (1 μg/site) significantly attenuated the CPP
effects of amphetamine infused into the NACC core. This
antagonism was also true for the cocaine-induced CPP in the NACC
shell. These results implied that the other cortical areas can
modulate such CPP effects, in particular the mPFC. In Eperiment
5, lesion of mPFC significantly inhibited the cocaine-induced
CPP in the shell area but not for the amphetamine-induced CPP in
the core area. Taken together, the NACC is an important neural
substrate for mediating the rewarding effects for amphetamine
and cocaine on the CPP task, and such effects can be dissociated
as drugs locally infused into core and shell areas.
Glutamatergic projections originating mPFC may provide some
motivational information to the NACC. The mPFC may distinctly
be involved in the motive circuit of cocaine- or amphetamine-
induced CPP in the NACC. These results highlight that different
processes are involved in the acquisition of CPP for
microinjection of amphetamine or cocaine into the NACC subareas.
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