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題名 Development of conditioned place preference induced by intra-accumbens infusion of amphetamine is attenuated by co-infusion of dopamine D1 and D2 receptor antagonists
作者 Liao, Ruey-Ming
廖瑞銘
貢獻者 國立政治大學心理學系
關鍵詞 Nucleus accumbens; Dopamine receptor subtypes; SCH23390; Raclopride; Drug reward; Place conditioning
日期 2008-03
上傳時間 29-Dec-2008 15:34:23 (UTC+8)
摘要 The present study investigated the role of dopamine receptors within the nucleus accumbens in place conditioning induced by D-amphetamine. Previous work has shown that conditioned place preference can be established by intra-accumbens infusion of amphetamine. The present study further examined whether bilateral co-infusion of the selective dopamine receptor antagonists with D-amphetamine into this region would disrupt the development of conditioned place preference induced by intra-accumbens amphetamine treatment. Bilateral infusions of D-amphetamine into the nucleus accumbens at the dose of 10 microg per side significantly induced conditioned place preference. At the tested doses of 1 microg and 10 microg, either the selective D1 dopamine receptor antagonist (SCH23390) or the selective D2 dopamine receptor antagonist (raclopride) infused with the high dose into the nucleus accumbens significantly blocked the development of conditioned place preference induced by intra-accumbens amphetamine treatment. Furthermore, the sole infusion of SCH23390 or raclopride into the nucleus accumbens produced little or no place conditioning effect. It is concluded that the dopamine D1 and D2 receptors in the nucleus accumbens are critically involved in the development of amphetamine induced conditioned place preference.
關聯 Pharmacology, Biochemistry and Behavior, 89(3), 367-373
資料類型 article
DOI http://dx.doi.org/10.1016/j.pbb.2008.01.009
dc.contributor 國立政治大學心理學系en_US
dc.creator (作者) Liao, Ruey-Mingen_US
dc.creator (作者) 廖瑞銘en_US
dc.date (日期) 2008-03en_US
dc.date.accessioned 29-Dec-2008 15:34:23 (UTC+8)-
dc.date.available 29-Dec-2008 15:34:23 (UTC+8)-
dc.date.issued (上傳時間) 29-Dec-2008 15:34:23 (UTC+8)-
dc.identifier.uri (URI) https://nccur.lib.nccu.edu.tw/handle/140.119/19816-
dc.description.abstract (摘要) The present study investigated the role of dopamine receptors within the nucleus accumbens in place conditioning induced by D-amphetamine. Previous work has shown that conditioned place preference can be established by intra-accumbens infusion of amphetamine. The present study further examined whether bilateral co-infusion of the selective dopamine receptor antagonists with D-amphetamine into this region would disrupt the development of conditioned place preference induced by intra-accumbens amphetamine treatment. Bilateral infusions of D-amphetamine into the nucleus accumbens at the dose of 10 microg per side significantly induced conditioned place preference. At the tested doses of 1 microg and 10 microg, either the selective D1 dopamine receptor antagonist (SCH23390) or the selective D2 dopamine receptor antagonist (raclopride) infused with the high dose into the nucleus accumbens significantly blocked the development of conditioned place preference induced by intra-accumbens amphetamine treatment. Furthermore, the sole infusion of SCH23390 or raclopride into the nucleus accumbens produced little or no place conditioning effect. It is concluded that the dopamine D1 and D2 receptors in the nucleus accumbens are critically involved in the development of amphetamine induced conditioned place preference.-
dc.format application/en_US
dc.language enen_US
dc.language en-USen_US
dc.language.iso en_US-
dc.relation (關聯) Pharmacology, Biochemistry and Behavior, 89(3), 367-373en_US
dc.subject (關鍵詞) Nucleus accumbens; Dopamine receptor subtypes; SCH23390; Raclopride; Drug reward; Place conditioning-
dc.title (題名) Development of conditioned place preference induced by intra-accumbens infusion of amphetamine is attenuated by co-infusion of dopamine D1 and D2 receptor antagonistsen_US
dc.type (資料類型) articleen
dc.identifier.doi (DOI) 10.1016/j.pbb.2008.01.009en_US
dc.doi.uri (DOI) http://dx.doi.org/10.1016/j.pbb.2008.01.009en_US