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首页> 外文期刊>The European Journal of Neuroscience >Novelty enhances retrieval: molecular mechanisms involved in rat hippocampus.
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Novelty enhances retrieval: molecular mechanisms involved in rat hippocampus.

机译:新颖性增强了检索:大鼠海马中涉及的分子机制。

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摘要

Rats exposed to a novel environment just prior to or 1-2 h, but not 4 or 6 h, before retention testing exhibited an enhanced retrieval of a one-trial inhibitory avoidance training. The bilateral intrahippocampal infusion of PD098059, an inhibitor of mitogen-activated protein kinase (MAPK), the specific upstream activator of p42 and p44 MAPKs, given 10 min before the exposure to the novel environment, blocked the enhancing effect of novelty on memory retrieval. In addition, prenovelty infusion of DL-2-amino-5-phosphonovalerate (APV), an antagonist of glutamate NMDA receptors, produced similar effects. The exposure to the novel environment is associated with an activation of p42 and p44 MAPKs and an increase in the phosphorylation state of the transcription factor cAMP response element binding protein (CREB). No changes were observed in cAMP-dependent protein kinase (PKA) activity or in alpha-CAMKII activation. Taken together, our results indicate that novelty activates hippocampal MAPKs, which are necessary, along with glutamate NMDA receptors, for the enhancing effect of novelty on retrieval.
机译:在保留测试之前或之后1-2小时,但不在4或6小时,暴露于新环境中的大鼠表现出增强的单试验抑制回避训练能力。在暴露于新环境之前10分钟,双侧海马输注PD098059(一种有丝分裂原激活的蛋白激酶(MAPK)的抑制剂),它是p42和p44 MAPKs的特异性上游激活剂,阻止了新奇对记忆恢复的增强作用。另外,谷氨酸NMDA受体的拮抗剂DL-2-氨基-5-膦酰戊二酸酯(APV)的新奇前期输注产生了相似的效果。暴露于新型环境与p42和p44 MAPKs的激活以及转录因子cAMP反应元件结合蛋白(CREB)的磷酸化状态增加有关。在cAMP依赖性蛋白激酶(PKA)活性或alpha-CAMKII激活中未观察到任何变化。两者合计,我们的结果表明,新颖性激活海马MAPK,这与谷氨酸NMDA受体一起对于增强新颖性对检索的作用是必需的。

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