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Reply to “Correspondence to Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder”

Molecular Psychiatry volume 25, pages 2205–2206 (2020)Cite this article

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We thank Chinopoulos [1] for his interest in our article [2] and valuable suggestions and for giving us a chance to become aware of our error. We cited the paper [3] reporting the opposite result caused by loss of Ant1 on calcium retention capacity (CRC) as reference 52. This citation should be re-numbered as reference 10. We apologize for any confusion caused by this error. We have submitted a corrigendum to notify this error.

We have had great interest in the paper from his group reporting that Ant1 is involved in voltage sensing of mitochondrial permeability transition pore (mPTP) in human fibroblasts and C2C12 myotubes [4]. As he pointed out, we did not measure other bioenergetics properties of brain mitochondria in Ant1 conditional knockout mice, except for CRC, and thus it was not clear whether altered CRC of brain mitochondria in Ant1 cKO mice was caused by the direct effect of the Ant1 mutation on mitochondrial bioenergetics.

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References

  1. Chinopoulos C. Correspondence to “Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder”. Mol. Psychiatry. 13 September 2018. https://www.nature.com/articles/s41380-018-0251-x

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Author notes

  1. Tomoaki M. Kato

    Present address: Department of Fundamental Cell Technology, Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan

Authors and Affiliations

  1. Laboratory for Molecular Dynamics of Mental Disorders, RIKEN Center for Brain Science, Wako, Japan

    Tadafumi Kato, Mie Kubota-Sakashita & Tomoaki M. Kato

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  1. Tadafumi Kato
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Correspondence to Tadafumi Kato.

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Kato, T., Kubota-Sakashita, M. & Kato, T.M. Reply to “Correspondence to Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder”. Mol Psychiatry 25, 2205–2206 (2020). https://doi.org/10.1038/s41380-018-0279-y

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