NV-5138 as a fast-acting antidepressant via direct activation of mTORC1 signaling
Yuto Hasegawa, Xiaolei Zhu, and Atsushi Kamiya
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Address correspondence to: Atsushi Kamiya, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Meyer 3-146, Baltimore, Maryland 21287, USA. Phone: 410.502.0060; Email: akamiya1@jhmi.edu.
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Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Address correspondence to: Atsushi Kamiya, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Meyer 3-146, Baltimore, Maryland 21287, USA. Phone: 410.502.0060; Email: akamiya1@jhmi.edu.
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Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Address correspondence to: Atsushi Kamiya, Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Meyer 3-146, Baltimore, Maryland 21287, USA. Phone: 410.502.0060; Email: akamiya1@jhmi.edu.
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First published May 20, 2019 - More info
J Clin Invest. 2019;129(6):2207–2209. https://doi.org/10.1172/JCI129702.
© 2019 American Society for Clinical Investigation
Growing evidence implicates altered mTORC1 signaling cascades in the pathophysiology of depression, suggesting that direct modulation of mTORC1 signaling may offer novel therapeutic potential. In this issue of the JCI, Kato and colleagues reported that administration of NV-5138, a recently developed synthetic leucine analog, has a rapid and sustained antidepressant action in rat models via activation of mTORC1 signaling. The investigators also found that the antidepressant effect of NV-5138 is mediated by upregulation of brain-derived neurotrophic factor (BDNF) signaling and that NV-5138 treatment produces rapid synaptic responses in the medial prefrontal cortex. These findings highlight the direct activation of mTORC1 signaling as a potential pharmacological intervention for the treatment of depression.
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