@inbook{9c3850b857754bc4b96f0bd5ca8348c0,
title = "BDNF receptor TRKB as a target of antidepressants",
abstract = "Accumulating evidence suggests that increased synthesis of the neurotrophin BDNF (brain-derived neurotrophic factor), activation of it{\textquoteright}s receptor TrkB (tropomyosin related kinase B), and subsequent facilitation of synaptogenesis and synaptic plasticity underlie the therapeutic effects of antidepressant treatments, including SSRIs (serotonin selective reuptake inhibitors) and the rapid-acting antidepressant ketamine. This review highlights some of the current knowledge (and open questions) about how mechanistically distinct treatments of depression may regulate BDNF-TrkB signaling in brain, and how this signaling pathway could be targeted with novel drugs carrying antidepressant potential. I will also introduce the network hypothesis of antidepressant action, a recently elaborated theorical framework that aims to understand the ultimate functional consequences of antidepressant-induced TrkB activation and plasticity. According to this hypothesis, antidepressants produce a heightened state of plasticity in the adult cortex which allows rewiring of neuronal connections when combined with rehabilitation. {\textcopyright} 2017 Nova Science Publishers, Inc.",
keywords = "3124 Neurology and psychiatry",
author = "T. Rantam{\"a}ki",
year = "2017",
language = "English",
isbn = "978-1-53611-980-0",
series = "Psychiatry – Theory, Applications and Treatments",
publisher = "Nova Science Publishers",
pages = "277--294",
editor = "Kim, \{Yong-Ku \}",
booktitle = "Major Depressive Disorder",
address = "United States",
}