BDNF receptor TRKB as a target of antidepressants

Forskningsoutput: Kapitel i bok/rapport/konferenshandlingKapitelVetenskapligPeer review

Sammanfattning

Accumulating evidence suggests that increased synthesis of the neurotrophin BDNF (brain-derived neurotrophic factor), activation of it’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. © 2017 Nova Science Publishers, Inc.
Originalspråkengelska
Titel på gästpublikationMajor Depressive Disorder : Risk Factors, Characteristics and Treatment Options
RedaktörerYong-Ku Kim
Antal sidor28
UtgivningsortNew York, NY
FörlagNova Science Publishers
Utgivningsdatum2017
Sidor277-294
ISBN (tryckt)978-1-53611-980-0
ISBN (elektroniskt)978-1-53612-003-5
StatusPublicerad - 2017
MoE-publikationstypA3 Del av bok eller annan forskningsbok

Publikationsserier

NamnPsychiatry – Theory, Applications and Treatments

Vetenskapsgrenar

  • 3124 Neurologi och psykiatri

Citera det här

Rantamäki, T. (2017). BDNF receptor TRKB as a target of antidepressants. I Y-K. Kim (Red.), Major Depressive Disorder: Risk Factors, Characteristics and Treatment Options (s. 277-294). (Psychiatry – Theory, Applications and Treatments). New York, NY: Nova Science Publishers.
Rantamäki, T. / BDNF receptor TRKB as a target of antidepressants. Major Depressive Disorder: Risk Factors, Characteristics and Treatment Options. redaktör / Yong-Ku Kim. New York, NY : Nova Science Publishers, 2017. s. 277-294 (Psychiatry – Theory, Applications and Treatments).
@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’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. {\circledC} 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",

}

Rantamäki, T 2017, BDNF receptor TRKB as a target of antidepressants. i Y-K Kim (red.), Major Depressive Disorder: Risk Factors, Characteristics and Treatment Options. Psychiatry – Theory, Applications and Treatments, Nova Science Publishers, New York, NY, s. 277-294.

BDNF receptor TRKB as a target of antidepressants. / Rantamäki, T.

Major Depressive Disorder: Risk Factors, Characteristics and Treatment Options. red. / Yong-Ku Kim. New York, NY : Nova Science Publishers, 2017. s. 277-294 (Psychiatry – Theory, Applications and Treatments).

Forskningsoutput: Kapitel i bok/rapport/konferenshandlingKapitelVetenskapligPeer review

TY - CHAP

T1 - BDNF receptor TRKB as a target of antidepressants

AU - Rantamäki, T.

PY - 2017

Y1 - 2017

N2 - Accumulating evidence suggests that increased synthesis of the neurotrophin BDNF (brain-derived neurotrophic factor), activation of it’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. © 2017 Nova Science Publishers, Inc.

AB - Accumulating evidence suggests that increased synthesis of the neurotrophin BDNF (brain-derived neurotrophic factor), activation of it’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. © 2017 Nova Science Publishers, Inc.

KW - 3124 Neurology and psychiatry

M3 - Chapter

SN - 978-1-53611-980-0

T3 - Psychiatry – Theory, Applications and Treatments

SP - 277

EP - 294

BT - Major Depressive Disorder

A2 - Kim, Yong-Ku

PB - Nova Science Publishers

CY - New York, NY

ER -

Rantamäki T. BDNF receptor TRKB as a target of antidepressants. I Kim Y-K, redaktör, Major Depressive Disorder: Risk Factors, Characteristics and Treatment Options. New York, NY: Nova Science Publishers. 2017. s. 277-294. (Psychiatry – Theory, Applications and Treatments).