Graphical Abstract: Antidepressant drugs act by directly binding to TrkB neurotrophin receptors. Source: Casarotto et al., 2021/open-access paper in Cell (CC BY 4.0) Key Points: A new study challenges previously held notions about how antidepressants work. This research suggests that slow-acting SSRIs and fast-acting ketamine bind directly to a brain-derived neurotrophic factor ( BDNF ) receptor and promote depression -alleviating neuronal plasticity without help from serotonin or glutamate. A new international study ( Casarotto et al., 2021 ) collaboratively led by senior author Eero Castrén of the University of Helsinki’s Neuroscience Center along with colleagues in the Department of Physics investigates how three different antidepressant drugs—fluoxetine (an SSRI sold under the brand name Prozac), imipramine (a tricyclic antidepressant), and rapid-acting ketamine (a new “breakthrough therapy ” for treatment-resistant depression; available only at a certified doctor’s office or clinic)—interact with a BDNF receptor known as TrkB. This open-access paper was published on February 18 in the peer-reviewed journal Cell . Historically, selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants’ effects were thought to be rooted in their ability to keep more serotonin and norepinephrine available to the brain by increasing levels of these neurotransmitters in the synaptic gap. Along this same line, the antidepressant effect… Read full this story
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