Memory formation is hypothesized to involve the generation of event-specific neural activity patterns during learning and the subsequent spontaneous reactivation of these patterns. Here, we present evidence that these processes can also be observed in urethane-anesthetized rats and are enhanced by desynchronized brain state evoked by tail pinch, subcortical carbachol infusion, or systemic amphetamine administration. During desynchronization, we found that repeated tactile or auditory stimulation evoked unique sequential patterns of neural firing in somatosensory and auditory cortex and that these patterns then reoccurred during subsequent spontaneous activity, similar to what we have observed in awake animals. Furthermore, the formation of these patterns was blocked by an NMDA receptor antagonist, suggesting that the phenomenon depends on synaptic plasticity. These results suggest that anesthetized animals with a desynchronized brain state could serve as a convenient model for studying stimulus-induced plasticity to improve our understanding of memory formation and replay in the brain.

译文

假设记忆形成涉及学习过程中事件特定的神经活动模式的产生以及这些模式的随后自发激活。在这里,我们提供的证据表明,这些过程也可以在氨基甲酸乙酯麻醉的大鼠中观察到,并因尾巴捏合,皮层下卡巴胆碱输注或全身苯丙胺给药引起的失调的大脑状态而得到增强。在去同步期间,我们发现反复的触觉或听觉刺激在体感和听觉皮层中引起了神经放电的独特顺序模式,然后这些模式在随后的自发活动中再次发生,类似于我们在清醒动物中观察到的情况。此外,NMDA受体拮抗剂阻止了这些模式的形成,表明该现象取决于突触可塑性。这些结果表明,具有失步的大脑状态的麻醉动物可以作为研究刺激诱导的可塑性的便捷模型,以增进我们对大脑记忆形成和重放的理解。

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