ArticleCommunications biology2025
Mineralocorticoid receptor knockout alters hippocampal CA2 neurons to become like those in CA1.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- A modifiable driver of dementia: cognitive impairment in primary aldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- From Synaptic Plasticity and Critical Periods to Social Behavior and Stress: Getting to, and Staying in, CA2.Hippocampus · 2026Review
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9 authors.
Funding
Abstract
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'.
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