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The NMDA receptor antagonist ketamine produces rapid and sustained antidepressant actions in depressed patients, but the underlying mechanisms, notably the role of vascular endothelial growth factor (VEGF) remain unclear. Here we use a combination of cell specific approaches to demonstrate that neuronal deletion of VEGF signaling blocks the antidepressant-like behavioral actions of ketamine and that infusion of VEGF into the medial prefrontal cortex is sufficient to produce antidepressant-like behavioral effects in rodent models. Together, these findings indicate that neuronal VEGF-Flk-1 signaling in the medial prefrontal cortex plays an essential role in the antidepressant actions of ketamine.
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This page is a summary of: Role of Neuronal VEGF Signaling in the Prefrontal Cortex in the Rapid Antidepressant Effects of Ketamine, American Journal of Psychiatry, May 2019, American Psychiatric Association,
DOI: 10.1176/appi.ajp.2018.17121368.
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