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Effects of intra-accumbal administration of dopamine and ionotropic glutamate receptor drugs on delay discounting performance in rats.
Behavioral Neuroscience ( IF 1.6 ) Pub Date : 2017-9-29 , DOI: 10.1037/bne0000214
Justin R Yates 1 , Michael T Bardo 1
Affiliation  

Nucleus accumbens core (NAcc) has been implicated in impulsive choice, as measured in delay discounting. The role of dopamine (DA) in impulsive choice has received considerable attention, whereas glutamate (Glu) has recently been shown to be an important mediator of discounting. However, research has not examined how DA or Glu receptors in NAcc mediate different aspects of delay discounting performance, that is, (a) sensitivity to reinforcer magnitude and (b) sensitivity to delayed reinforcement. Adult male Sprague-Dawley rats were first trained in a delay discounting task, in which the delay to a large magnitude food reinforcer increased across blocks of trials. Following behavioral training, rats received bilateral implantation of guide cannulas into NAcc. Half of the rats (n = 12) received infusions of the DA-selective ligands SKF 38393 (D1-like agonist: 0.03 or 0.1 μg), SCH 23390 (D1-like antagonist: 0.3 or 1.0 μg), quinpirole (D2-like agonist: 0.3 or 1.0 μg), and eticlopride (D2-like antagonist: 0.3 or 1.0 μg). The other half received infusions of the ionotropic Glu ligands MK-801 (NMDA uncompetitive antagonist: 0.3 or 1.0 μg), AP-5 (NMDA competitive antagonist: 0.3 or 1.0 μg), ifenprodil (noncompetitive antagonist at NR2B-containing NMDA receptors: 0.3 or 1.0 μg), and CNQX (AMPA competitive antagonist: 0.2 or 0.5 μg). Results showed that SCH 23390 (0.3 μg) decreased sensitivity to reinforcer magnitude without altering impulsive choice, whereas ifenprodil (1.0 μg) decreased sensitivity to delayed reinforcement (i.e., impulsive choice). The current results show that DA and NMDA receptors in NAcc mediate distinct aspects of discounting performance. (PsycINFO Database Record

中文翻译:


多巴胺和离子型谷氨酸受体药物的室内给药对大鼠延迟贴现性能的影响。



通过延迟贴现来衡量,伏隔核 (NAcc) 与冲动选择有关。多巴胺(DA)在冲动选择中的作用受到了相当多的关注,而谷氨酸(Glu)最近被证明是折扣的重要中介。然而,研究尚未检验 NAcc 中的 DA 或 Glu 受体如何介导延迟折扣性能的不同方面,即 (a) 对强化强度的敏感性和 (b) 对延迟强化的敏感性。成年雄性斯普拉格-道利大鼠首先接受延迟折扣任务训练,其中大量食物强化剂的延迟在试验中不断增加。行为训练后,大鼠接受双侧引导插管植入 NAcc。一半大鼠 (n = 12) 接受 DA 选择性配体 SKF 38393(D1 样激动剂:0.03 或 0.1 μg)、SCH 23390(D1 样拮抗剂:0.3 或 1.0 μg)、喹吡罗(D2 样)输注激动剂:0.3 或 1.0 μg)和艾氯必利(D2 样拮抗剂:0.3 或 1.0 μg)。另一半接受离子型 Glu 配体 MK-801(NMDA 非竞争性拮抗剂:0.3 或 1.0 μg)、AP-5(NMDA 竞争性拮抗剂:0.3 或 1.0 μg)、艾芬地尔(含 NR2B NMDA 受体的非竞争性拮抗剂:0.3)输注或 1.0 μg)和 CNQX(AMPA 竞争性拮抗剂:0.2 或 0.5 μg)。结果表明,SCH 23390 (0.3 μg) 降低了对强化强度的敏感性,但不改变冲动选择,而艾芬地尔 (1.0 μg) 降低了对延迟强化(即冲动选择)的敏感性。目前的结果表明,NAcc 中的 DA 和 NMDA 受体介导折扣性能的不同方面。 (PsycINFO 数据库记录
更新日期:2020-08-21
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