Commentary 10.1172/JCI129702
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.
Find articles by Hasegawa, Y. in: JCI | PubMed | Google Scholar
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.
Find articles by
Zhu, X.
in:
JCI
|
PubMed
|
Google Scholar
|
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.
Find articles by
Kamiya, A.
in:
JCI
|
PubMed
|
Google Scholar
|
First published May 20, 2019 - More info
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.
A subscription is required for you to read this article in full. If you are a subscriber, you may sign in to continue reading.
Click here to sign into your account.
Please select one of the subscription options, which includes a low-cost option just for this article.
If you are at an institution or library and believe you should have access, please check with your librarian or administrator (more information).
Please try these troubleshooting tips.