Mineralocorticoid receptors (MRs) in the brain play a role in learning and memory, neuronal differentiation, and regulation of the stress response. Within the hippocampus, the highest expression of MRs is in area CA2. CA2 pyramidal neurons have a distinct molecular makeup resulting in a plasticity-resistant phenotype, distinguishing them from neurons in CA1 and CA3. Thus, we asked whether MRs regulate CA2 neuron properties and CA2-related behaviors. Using three conditional knockout methods at different stages of development, we found a striking decrease in multiple molecular markers for CA2, an effect mimicked by chronic antagonism of MRs. Furthermore, embryonic deletion of MRs disrupted afferent inputs to CA2 and enabled synaptic potentiation of the normally LTP-resistant synaptic currents in CA2. We also found that CA2-targeted MR knockout was sufficient to disrupt social behavior and alter behavioral responses to novelty. Altogether, these results demonstrate an unappreciated role for MRs in controlling CA2 pyramidal cell identity and in facilitating CA2-dependent behaviors.

中文翻译：

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盐皮质激素受体在控制神经元表型中的新作用。

大脑中的盐皮质激素受体 (MR) 在学习和记忆、神经元分化和应激反应调节中发挥作用。在海马内，MR 的最高表达位于 CA2 区。CA2 锥体神经元具有独特的分子组成，导致可塑性抵抗表型，将其与 CA1 和 CA3 中的神经元区分开来。因此，我们询问 MR 是否调节 CA2 神经元特性和 CA2 相关行为。在不同的发育阶段使用三种条件敲除方法，我们发现 CA2 的多个分子标记物显着减少，这种效应类似于 MR 的长期拮抗作用。此外，胚胎时期 MR 的缺失破坏了 CA2 的传入输入，并使 CA2 中通常耐 LTP 的突触电流得以增强。我们还发现 CA2 靶向 MR 敲除足以扰乱社会行为并改变对新奇事物的行为反应。总而言之，这些结果表明 MR 在控制 CA2 锥体细胞身份和促进 CA2 依赖性行为方面的作用未被充分认识。