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在小鼠中定向删除GluR-1 AMPA受体可分离出食欲性奖励对学习的一般影响和特定结果影响。

Targeted deletion of the GluR-1 AMPA receptor in mice dissociates general and outcome-specific influences of appetitive rewards on learning.

作者信息

Johnson Alexander W, Bannerman David, Rawlins Nick, Sprengel Rolf, Good Mark A

机构信息

School of Psychology, Cardiff University, UK.

出版信息

Behav Neurosci. 2007 Dec;121(6):1192-202. doi: 10.1037/0735-7044.121.6.1192.

Abstract

The authors assessed the hypothesis that deletion of the GluR-1 subtype of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptor in mice disrupts the associative activation of a sensory-specific representation of an appetitive reward. In Experiment 1, mice received training on a Pavlovian-instrumental transfer task. In the test stage, conditioned stimulus (CS) presentations enhanced instrumental actions in both groups. However, this effect was specific to the action that shared the same outcome as the CS in wild-type (WT), but not GluR-1-super(-/-), mice. In Experiment 2, the mice were trained on a heterogeneous instrumental chain in which rewards were obtained for emitting 1 response (R1, that was distal to reward delivery), followed by a 2nd response (R2, that was proximal to reward delivery). A change in general motivational state (from hungry to sated) reduced the number of R2 responses in both groups. In contrast, an outcome-specific satiety treatment produced a selective decline in R1 responding only in WT mice. The results support the hypothesis that GluR-1 deletion impairs the associative activation of a representation of the sensory-specific incentive motivational properties of an appetitive reward.

摘要

作者评估了以下假设

小鼠体内α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体的GluR-1亚型缺失会破坏对食欲性奖赏的感觉特异性表征的联合激活。在实验1中,小鼠接受了巴甫洛夫式工具性转移任务的训练。在测试阶段,条件刺激(CS)呈现增强了两组小鼠的工具性动作。然而,在野生型(WT)小鼠中,这种效应特定于与CS具有相同结果的动作,但在GluR-1基因敲除(GluR-1-/-)小鼠中并非如此。在实验2中,小鼠接受了异质工具链训练,其中发出1次反应(R1,距离奖赏发放较远),接着是第2次反应(R2,距离奖赏发放较近)可获得奖赏。一般动机状态的改变(从饥饿到饱腹)减少了两组小鼠的R2反应次数。相比之下,结果特异性饱腹感处理仅使WT小鼠的R1反应选择性下降。这些结果支持了以下假设:GluR-1缺失会损害对食欲性奖赏的感觉特异性激励动机属性表征的联合激活。

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