PerspectiveNeuroscience

Do antidepressants restore lost synapses?

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Science  12 Apr 2019:
Vol. 364, Issue 6436, pp. 129-130
DOI: 10.1126/science.aax0719

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Summary

Depression is a mental illness characterized by episodes of a sad, despondent mood and/or a loss of interest or pleasure (1). This pathology affects nearly 20% of the population in the United States (2), and treatments are limited. Indeed, in the 5 years following remission, 80% of patients will endure relapse and more than 30% of patients suffer from treatment-resistant depression. Recently, the U.S. Food and Drug Administration (FDA) approved the clinical use of esketamine nasal spray for depression that is resistant to other treatments (3). Esketamine is an enantiomer of ketamine, a drug with antidepressant properties, although its mechanism of action remains unclear. Brain imaging studies suggest that neuronal circuitry in the medial prefrontal cortex (mPFC) is involved in the physiopathology of this disorder (4). On page 147 of this issue, Moda-Sava et al. (5) report that ketamine induces plasticity of dendritic spines on mPFC neurons and restores microcircuit activity and behavior in animal models of depression. This may expand therapeutic strategies for treating major depression.

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