Answers are grounded in this paper and cite their sources.
Spatial transcriptomics reveals that mineralocorticoid receptor deletion shifts hippocampal CA2 neurons toward a CA1-like fate in mice, indicating receptor control over regional neuronal identity.
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 used a spatial transcriptomics approach. We found that without MRs, ‘CA2’ neurons acquire a CA1-like molecular phenotype. Additionally, we found that neurons in this area appear to have a cell size and density more like that in CA1. These finding support the idea that MRs control at least CA2’s ‘state’ during development, resulting in a CA1-like ‘fate’.
No takes yet. Share an insight, caveat, or question.
Harris et al. (2024) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: