Effects of stress and hippocampal NMDA receptor antagonism on recognition memory in rats
Effects of stress and hippocampal NMDA receptor antagonism on recognition memory in rats
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DOI：
10.1101/lm.46102
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发表时间：
2002-03-01
影响因子：
2
通讯作者：
Kim, JJ
中科院分区：
文献类型：
--
作者：
Baker, KB;Kim, JJ
暴露于无法控制的压力已被证明会改变随后在海马突触可塑性和干扰海马依赖的空间记忆大鼠。本研究通过大鼠视觉配对比较任务（VPC）测试，探讨了损害海马长时程增强（LTP）的应激是否也影响（非空间）海马依赖性物体识别记忆。在经历了一个不可避免的限制tailshock压力的经验，大鼠表现出显着受损的识别记忆在3小时（长）熟悉测试相延迟，但不是在5分钟（短）延迟。相比之下，无压力的对照动物显示出稳健的识别记忆（即，它们在短延迟期和长延迟期都表现出对新奇事物的可靠偏好。应激对长延迟再认记忆的损害作用是短暂的，因为在经历应激体验后48 h，动物在长延迟时表现正常。与应激相似，将DL-2-氨基-5-膦酰基戊酸（APV）（一种阻断LTP的竞争性N-甲基-D-天冬氨酸受体（NMDAR）拮抗剂）微量输注到背侧海马中选择性地损害了长延迟期的物体识别记忆。总之，这些结果表明，压力和海马内施用APV通过影响海马中的突触可塑性来影响识别记忆。
Exposures to uncontrollable stress have been shown to alter ensuing synaptic plasticity in the hippocampus and interfere with hippocampal-dependent spatial memory in rats. The present study examined whether stress, which impairs hippocampal long-term potentiation (LTP), also affects (nonspatial) hippocampal-dependent object-recognition memory, as tested on the visual paired comparison task (VPC) in rats. After undergoing an inescapable restraint-tailshock stress experience, rats exhibited markedly impaired recognition memory at the 3-h (long) familiarization-to-test phase delay but not at the 5-min (short) delay. In contrast, unstressed control animals showed robust recognition memory (i.e., they exhibited reliable preferences for novel over familiar objects) at both short- and long-delay periods. The impairing effect of stress on long-delay recognition memory was transient because 48 h after undergoing stress experience, animals performed normally at the long delay. Similar to stress, microinfusions of DL-2-amino-5-phosphonovaleric acid (APV), a competitive N-methyl-D-aspartate receptor (NMDAR) antagonist that blocks LTP, into the dorsal hippocampus selectively impaired object-recognition memory at the long-delay period. Together, these results suggest that stress and intrahippocampal administration of APV affect recognition memory by influencing synaptic plasticity in the hippocampus.