ArticleMolecular medicine (Cambridge, Mass.)2026
Mitochondrial Calcium Uniporter protects hippocampal CA2 neurons from NMDA-induced excitotoxic injury.
Article in Molecular medicine (Cambridge, Mass.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundThe hippocampal region CA2, unlike neighboring CA1, is exceptionally resistant to excitotoxicity, although the mechanisms behind this phenotype are unknown. Given the importance of mitochondrial calcium buffering, we investigated whether Mitochondrial Calcium Uniporter (MCU), known to be enriched in CA2, contributes to this resistance.
methodsWe employed immunostaining techniques in rodent brain tissue and organotypic slice cultures to visualize MCU across hippocampal regions under resting and excitotoxic conditions. Subsequently, we pharmacologically modulated MCU in an organotypic model of hippocampal excitotoxicity to assess its contribution to regional resistance.
resultsWe found a strong spatial correlation between resistance to NMDA excitotoxic injury and MCU expression. NMDA exposure resulted in MCU upregulation in CA2, and pharmacological inhibition of MCU sensitized CA2 neurons to excitotoxic damage in a dose-dependent manner, while having minimal effect on the already vulnerable CA1 neurons, which express low MCU levels.
conclusionsMCU is known to exacerbate NMDA-induced cell injury, although our data demonstrate a functional association between MCU activity and CA2 neuroprotection, suggesting that CA2 neurons may possess unique mitochondrial calcium handling capabilities. Our study provides novel insight into mechanisms supporting CA2 resistance to NMDA excitotoxic death and emphasizes context-dependent roles of MCU in neuronal injury or survival.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.