Prior learning can modify the plasticity mechanisms that are used to encode new information. For example, NMDA receptor (NMDAR) activation is typically required for new spatial and contextual learning in the hippocampus. However, once animals have acquired this information, they can learn new tasks even if NMDARs are blocked. This finding suggests that behavioral training alters cellular plasticity mechanisms such that NMDARs are not required for subsequent learning. The mechanisms that mediate this change are currently unknown. To address this issue, we tested the idea that changes in intrinsic excitability (induced by learning) facilitate the encoding of new memories via metabotropic glutamate receptor (mGluR) activation. Consistent with this hypothesis, hippocampal neurons exhibited increases in intrinsic excitability after learning that lasted for several days. This increase was selective and only observed in neurons that were activated by the learning event. When animals were trained on a new task during this period, excitable neurons were reactivated and memory formation required the activation of mGluRs instead of NMDARs. These data suggest that increases in intrinsic excitability may serve as a metaplastic mechanism for memory formation.

中文翻译：

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元可塑性有助于海马中的记忆形成。

先验学习可以修改用于编码新信息的可塑性机制。例如，NMDA 受体 (NMDAR) 激活通常是海马中新的空间和上下文学习所必需的。然而，一旦动物获得了这些信息，即使 NMDAR 被阻止，它们也可以学习新任务。这一发现表明，行为训练改变了细胞可塑性机制，因此后续学习不需要 NMDAR。调解这种变化的机制目前尚不清楚。为了解决这个问题，我们测试了内在兴奋性的变化（由学习引起）通过代谢型谷氨酸受体 (mGluR) 激活促进新记忆编码的想法。与这个假设一致，海马神经元在持续数天的学习后表现出内在兴奋性的增加。这种增加是选择性的，并且仅在被学习事件激活的神经元中观察到。当动物在此期间接受一项新任务的训练时，可兴奋的神经元被重新激活，记忆形成需要激活 mGluR 而不是 NMDAR。这些数据表明，内在兴奋性的增加可能是记忆形成的化生机制。