<p>Hippocampal area CA2 has emerged as a functionally and molecularly distinct part of the hippocampus and is necessary for several types of social behavior including social aggression. As part of the unique molecular profile of both mouse and human CA2, the mineralocorticoid receptor (MR; <i>Nr3c2</i>) appears to play a critical role in controlling CA2 neuron cellular and synaptic properties. To better understand the fate (or state) of the neurons resulting from MR conditional knockout, we use a spatial transcriptomics approach. We find that without MRs, ‘CA2’ neurons acquire a CA1-like molecular phenotype. Additionally, we find that neurons in this area appear to have a cell size and density more like that in CA1. These findings support the idea that MRs control CA2’s ‘state’, at least during development, resulting in a CA1-like ‘fate’.</p>

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Mineralocorticoid receptor knockout alters hippocampal CA2 neurons to become like those in CA1

  • Erin P. Harris,
  • Başak Kandemir,
  • Stephanie M. Jones,
  • Georgia M. Alexander,
  • James M. Ward,
  • TianYuan Wang,
  • Stephanie Proaño,
  • Xin Xu,
  • Serena M. Dudek

摘要

Hippocampal area CA2 has emerged as a functionally and molecularly distinct part of the hippocampus and is necessary for several types of social behavior including social aggression. As part of the unique molecular profile of both mouse and human CA2, the mineralocorticoid receptor (MR; Nr3c2) appears to play a critical role in controlling CA2 neuron cellular and synaptic properties. To better understand the fate (or state) of the neurons resulting from MR conditional knockout, we use a spatial transcriptomics approach. We find that without MRs, ‘CA2’ neurons acquire a CA1-like molecular phenotype. Additionally, we find that neurons in this area appear to have a cell size and density more like that in CA1. These findings support the idea that MRs control CA2’s ‘state’, at least during development, resulting in a CA1-like ‘fate’.