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奖赏性记忆再巩固依赖于NMDA受体介导的神经传递。

Appetitive memory reconsolidation depends upon NMDA receptor-mediated neurotransmission.

作者信息

Lee Jonathan L C, Everitt Barry J

机构信息

Behavioural and Clinical Neuroscience Institute, Department of Experimental Psychology, University of Cambridge, Downing Street, Cambridge CB2 3EB, UK.

出版信息

Neurobiol Learn Mem. 2008 Jul;90(1):147-54. doi: 10.1016/j.nlm.2008.02.004. Epub 2008 Mar 26.

Abstract

Memory persistence is a dynamic process involving the reconsolidation of memories after their reactivation. Reconsolidation impairments have been demonstrated for many types of memories in rats, and signaling at N-methyl-d-aspartate (NMDA) receptors appears often to be a critical pharmacological mechanism. Here we investigated the reconsolidation of appetitive pavlovian memories reinforced by natural rewards. In male Lister Hooded rats, systemic administration of the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-SH-dibenzo{a,d}cyclohepten-5,10-imine maleate (MK-801, 0.1mg/kg i.p.) either before or immediately following a brief memory reactivation session abolished the subsequent acquisition of a new instrumental response with sucrose conditioned reinforcement. However, only when injected prior to memory reactivation was MK-801 effective in disrupting the maintenance of a previously-acquired instrumental response with conditioned reinforcement. These results demonstrate that NMDA receptor-mediated signaling is required for appetitive pavlovian memory reconsolidation.

摘要

记忆的持久性是一个动态过程,涉及记忆重新激活后的再巩固。在大鼠中,多种类型的记忆都已证明存在再巩固障碍,N-甲基-D-天冬氨酸(NMDA)受体处的信号传导似乎常常是一种关键的药理学机制。在此,我们研究了由自然奖励强化的经典性条件反射记忆的再巩固。在雄性利斯特戴帽大鼠中,在短暂的记忆重新激活阶段之前或之后立即全身注射NMDA受体拮抗剂(+)-5-甲基-10,11-二氢-5H-二苯并[a,d]环庚烯-5,10-亚胺马来酸盐(MK-801,0.1mg/kg腹腔注射),会消除随后通过蔗糖条件强化获得新的操作性反应的能力。然而,只有在记忆重新激活之前注射时,MK-801才有效破坏先前获得的通过条件强化的操作性反应的维持。这些结果表明,NMDA受体介导的信号传导是经典性条件反射记忆再巩固所必需的。

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