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題名 Examination of the effects of SCH23390 and raclopride infused in the dorsal striatum on amphetamine-induced timing impulsivity measured on a differential reinforcement of low-rate responding (DRL) task in rats
作者 廖瑞銘
Liao, Ruey-Ming
Cheng, Ruey-Kuang
貢獻者 心理系
關鍵詞 Impulsive action ; Behavioral inhibition ; Timing
日期 2019-11
上傳時間 2-十二月-2019 15:57:03 (UTC+8)
摘要 Although the striatal dopamine (DA) is reportedly involved in impulsive action, little is known about the DA subtype receptors of dorsal striatum (dSTR) in the impulsive control involved in differential reinforcement of low-rate-responding (DRL) behavior. We examined the receptor-specific dopaminergic modulation of d-amphetamine (AMP)-altered DRL 10 s (DRL-10 s) performance by locally infusing SCH23390 (SCH) and raclopride (RAC), DA D1 and D2 receptor antagonists, respectively, into the rat’s dSTR. Systemic injection of AMP significantly affected DRL-10 s behavior by increasing total, non-reinforced, and bust responses, as well as by decreasing reinforced responses, which correspondingly caused a leftward shift of the inter-response-time distribution curve as confirmed by a profound decrease in peak time (i.e., < 10 s). Neither SCH nor RAC into dSTR pharmacologically reversed the timing impulsivity produced by AMP as measured by non-reinforced responses and peak time. However, the increase in total responses and the decrease in reinforced responses by AMP were reversed by intra-dSTR SCH or RAC. These results suggest that the D1 and D2 receptors of the dSTR may be involved in behavioral components apart from the timing impulsivity produced by AMP on a DRL task, which components are distinctly different from those in other terminal areas of midbrain DA systems
關聯 Behavioural Brain Research, 2019 Nov 15:112364.
資料類型 article
DOI https://doi.org/10.1016/j.bbr.2019.112364
dc.contributor 心理系-
dc.creator (作者) 廖瑞銘-
dc.creator (作者) Liao, Ruey-Ming-
dc.creator (作者) Cheng, Ruey-Kuang-
dc.date (日期) 2019-11-
dc.date.accessioned 2-十二月-2019 15:57:03 (UTC+8)-
dc.date.available 2-十二月-2019 15:57:03 (UTC+8)-
dc.date.issued (上傳時間) 2-十二月-2019 15:57:03 (UTC+8)-
dc.identifier.uri (URI) http://nccur.lib.nccu.edu.tw/handle/140.119/127646-
dc.description.abstract (摘要) Although the striatal dopamine (DA) is reportedly involved in impulsive action, little is known about the DA subtype receptors of dorsal striatum (dSTR) in the impulsive control involved in differential reinforcement of low-rate-responding (DRL) behavior. We examined the receptor-specific dopaminergic modulation of d-amphetamine (AMP)-altered DRL 10 s (DRL-10 s) performance by locally infusing SCH23390 (SCH) and raclopride (RAC), DA D1 and D2 receptor antagonists, respectively, into the rat’s dSTR. Systemic injection of AMP significantly affected DRL-10 s behavior by increasing total, non-reinforced, and bust responses, as well as by decreasing reinforced responses, which correspondingly caused a leftward shift of the inter-response-time distribution curve as confirmed by a profound decrease in peak time (i.e., < 10 s). Neither SCH nor RAC into dSTR pharmacologically reversed the timing impulsivity produced by AMP as measured by non-reinforced responses and peak time. However, the increase in total responses and the decrease in reinforced responses by AMP were reversed by intra-dSTR SCH or RAC. These results suggest that the D1 and D2 receptors of the dSTR may be involved in behavioral components apart from the timing impulsivity produced by AMP on a DRL task, which components are distinctly different from those in other terminal areas of midbrain DA systems-
dc.format.extent 1503994 bytes-
dc.format.mimetype application/pdf-
dc.relation (關聯) Behavioural Brain Research, 2019 Nov 15:112364.-
dc.subject (關鍵詞) Impulsive action ; Behavioral inhibition ; Timing-
dc.title (題名) Examination of the effects of SCH23390 and raclopride infused in the dorsal striatum on amphetamine-induced timing impulsivity measured on a differential reinforcement of low-rate responding (DRL) task in rats-
dc.type (資料類型) article-
dc.identifier.doi (DOI) 10.1016/j.bbr.2019.112364-
dc.doi.uri (DOI) https://doi.org/10.1016/j.bbr.2019.112364-