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随后的自发重新激活。在这里,我们提供的证据表明,这些过程也可以在氨基甲酸酯麻醉的大鼠中观察到,并且通过尾巴捏合,皮质下卡巴胆碱输注或全身苯丙胺给药引起的不同步的大脑状态而增强。在去同步化过程中,我们发现反复的触觉或听觉刺激诱发了体感和听觉皮层中神经放电的独特顺序模式,并且这些模式随后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,这些模式的形成被NMDA受体拮抗剂阻断,表明该现象取决于突触可塑性。这些结果表明,大脑状态不同步的麻醉动物可以作为研究刺激诱导的可塑性的方便模型,以提高我们对大脑中记忆形成和重放的理解。

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