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Piia Kohtala

Bio: Piia Kohtala is an academic researcher from University of Helsinki. The author has contributed to research in topics: Tropomyosin receptor kinase B. The author has co-authored 1 publications.

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31 Aug 2021-bioRxiv
TL;DR: In this paper, both pharmacological and non-pharmacological treatments of depression activate TrkB receptors by inducing a physiological response coupled to sedation, and the authors suggest that the phenomenon underlying TrkB transactivation is essential but not sufficient, for antidepressant responses.
Abstract: We show that both pharmacological and non-pharmacological treatments of depression activate TrkB receptors - a well-established target of antidepressants - by inducing a physiological response coupled to sedation. Several rapid-acting antidepressants trigger TrkB signaling by evoking a state associated with electroencephalographic slow-wave activity, behavioral immobility, reduced cerebral glucose utilization, and lowered body temperature. Remarkably, antidepressant-induced TrkB signaling was not compromised in animals exhibiting reduced activity-dependent release of BDNF but was diminished by maintaining animals in warm ambient temperature. Most importantly, prevention of the hypothermic response attenuated the behavioral effects produced by rapid-acting antidepressant nitrous oxide. Our results suggest that the phenomenon underlying TrkB transactivation - changes in energy expenditure and thermoregulation - is essential, but not sufficient, for antidepressant responses. Indeed, regardless of differential clinical and pharmacodynamic properties, all drugs that disrupt energy metabolism and induce hypothermia activated TrkB. This study challenges pharmacology-centric hypotheses regarding antidepressant effects and highlight the role of complex changes in bioenergetics and thermoregulation.