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Requirement of AMPK activation for neuronal metabolic-enhancing effects of antidepressant paroxetine

Authors
 Jihyeon Jeong  ;  Minsun Park  ;  Jeong Seon Yoon  ;  Hyunjeong Kim  ;  Su Kyoung Lee  ;  Eun Lee  ;  Kee Namkoong  ;  Eosu Kim 
Citation
 Neuroreport, Vol.26(7) : 424-428, 2015 
Journal Title
 Neuroreport 
ISSN
 0959-4965 
Issue Date
2015
MeSH
AMP-Activated Protein Kinases/antagonists & inhibitors ; AMP-Activated Protein Kinases/metabolism* ; Adenosine Triphosphate/metabolism ; Antidepressive Agents/pharmacology* ; Cell Line, Tumor ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Energy Metabolism/drug effects ; Glucose/metabolism ; Humans ; Mitochondria/drug effects ; Mitochondria/metabolism ; Neurons/drug effects* ; Neurons/metabolism* ; Organelle Biogenesis ; Paroxetine/pharmacology* ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Serotonin Uptake Inhibitors/pharmacology* ; Transcription Factors/metabolism
Abstract
Reduced glucose metabolism has been implicated as a pathophysiology of depressive disorder. Normalization of such impaired neurometabolism has been related to the therapeutic actions of antidepressant medication. However, the molecular mechanism underlying the neurometabolic actions of antidepressants has not been fully understood. Given that AMP-activated protein kinase (AMPK) is a master switch for energy homeostasis, we aimed to determine whether selective serotonin reuptake inhibitor paroxetine enhances energy metabolism by activating AMPK in neuroblastoma cells. We found that paroxetine dose dependently increased mitochondrial biogenesis, which involves the AMPK-peroxisome proliferator-activated receptor-γ coactivator-1α pathway. In addition, paroxetine-induced AMPK activation increases glucose uptake and ATP production. These neurometabolic effects of paroxetine were suppressed by cotreatment with compound C (CC), an AMPK inhibitor. These findings suggest a possibility that modulation of the AMPK pathway might be a previously unrecognized mechanism underlying the neurometabolic action of antidepressants. Further study is warranted to examine the region-specific and time-specific effects of AMPK modulation by antidepressants on mood-related behaviors.
Full Text
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00001756-201505010-00007&LSLINK=80&D=ovft
DOI
10.1097/WNR.0000000000000365
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Psychiatry (정신과학교실) > 1. Journal Papers
Yonsei Authors
김어수(Kim, Eosu) ORCID logo https://orcid.org/0000-0001-9472-9465
남궁기(Namkoong, Kee) ORCID logo https://orcid.org/0000-0003-1400-8057
이은(Lee, Eun) ORCID logo https://orcid.org/0000-0002-7462-0144
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/157244
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