Active dendritic integrative mechanisms such as regenerative dendritic spikes enrich the information processing abilities of neurons and fundamentally contribute to behaviorally relevant computations. Dendritic Ca 2+ spikes are generally thought to produce plateau-like dendritic depolarization and somatic complex spike burst (CSB) firing, which can initiate rapid changes in spatial coding properties of hippocampal pyramidal cells (PCs). However, here we reveal that a morpho-topographically distinguishable subpopulation of rat and mouse hippocampal CA3PCs exhibits compound apical dendritic Ca 2+ spikes with unusually short duration that do not support the firing of sustained CSBs. These Ca 2+ spikes are mediated by L-type Ca 2+ channels and their time course is restricted by A- and M-type K + channels. Cholinergic activation powerfully converts short Ca 2+ spikes to long-duration forms, and facilitates and prolongs CSB firing. We propose that cholinergic neuromodulation controls the ability of a CA3PC subtype to generate sustained plateau potentials, providing a state-dependent dendritic mechanism for memory encoding and retrieval.

中文翻译：

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树突状 Ca 2+ 刺突的胆碱能调节控制海马 CA3 锥体神经元的放电模式


活跃的树突整合机制，如再生树突尖峰，丰富了神经元的信息处理能力，并从根本上促进了行为相关的计算。树突状 Ca 2+ 刺突通常被认为会产生高原状树突去极化和体细胞复合体刺突爆发 （CSB） 放电，这可以引发海马锥体细胞 （PCs） 空间编码特性的快速变化。然而，在这里我们揭示了大鼠和小鼠海马 CA3PCs 的形态地形学可区分亚群表现出复合的顶端树突状 Ca 2+ 尖峰，持续时间异常短，不支持持续 CSB 的放电。这些 Ca 2+ 尖峰由 L 型 Ca 2+ 通道介导，其时间过程受 A 型和 M 型 K + 通道的限制。胆碱能激活有力地将短的 Ca 2+ 尖峰转化为长持续时间的形式，并促进和延长 CSB 放电。我们提出胆碱能神经调控控制 CA3PC 亚型产生持续平台电位的能力，为记忆编码和检索提供状态依赖性树突机制。