Is glycogen synthase kinase-3 a central modulator in mood regulation

Xiaohua Li, Richard S Jope

Research output: Contribution to journalArticle

181 Citations (Scopus)

Abstract

Little is known regarding the mechanisms underlying the complex etiology of mood disorders, represented mainly by major depressive disorder and bipolar disorder. The 1996 discovery that lithium inhibits glycogen synthase kinase-3 (GSK3) raised the possibility that impaired inhibition of GSK3 is associated with mood disorders. This is now supported by evidence from animal biochemical, pharmacological, molecular, and behavioral studies and from human post-mortem brain, peripheral tissue, and genetic studies that are reviewed here. Mood disorders may result in part from impairments in mechanisms controlling the activity of GSK3 or GSK3-regulated functions, and disruptions of these regulating systems at different signaling sites may contribute to the heterogeneity of mood disorders. This substantial evidence supports the conclusion that bolstering the inhibitory control of GSK3 is an important component of the therapeutic actions of drugs used to treat mood disorders and that GSK3 is a valid target for developing new therapeutic interventions.

Original languageEnglish
Pages (from-to)2143-2154
Number of pages12
JournalNeuropsychopharmacology
Volume35
Issue number11
DOIs
StatePublished - Oct 1 2010
Externally publishedYes

Fingerprint

Glycogen Synthase Kinase 3
Mood Disorders
Major Depressive Disorder
Bipolar Disorder
Lithium
Pharmacology
Brain
Therapeutics
Pharmaceutical Preparations

Keywords

  • glycogen synthase kinase-3
  • lithium
  • molecular and cellular neurobiology
  • mood disorders
  • neuropharmacology
  • signal transduction

ASJC Scopus subject areas

  • Pharmacology
  • Psychiatry and Mental health

Cite this

Is glycogen synthase kinase-3 a central modulator in mood regulation. / Li, Xiaohua; Jope, Richard S.

In: Neuropsychopharmacology, Vol. 35, No. 11, 01.10.2010, p. 2143-2154.

Research output: Contribution to journalArticle

@article{2556edf7e720411ea06e89477038262b,
title = "Is glycogen synthase kinase-3 a central modulator in mood regulation",
abstract = "Little is known regarding the mechanisms underlying the complex etiology of mood disorders, represented mainly by major depressive disorder and bipolar disorder. The 1996 discovery that lithium inhibits glycogen synthase kinase-3 (GSK3) raised the possibility that impaired inhibition of GSK3 is associated with mood disorders. This is now supported by evidence from animal biochemical, pharmacological, molecular, and behavioral studies and from human post-mortem brain, peripheral tissue, and genetic studies that are reviewed here. Mood disorders may result in part from impairments in mechanisms controlling the activity of GSK3 or GSK3-regulated functions, and disruptions of these regulating systems at different signaling sites may contribute to the heterogeneity of mood disorders. This substantial evidence supports the conclusion that bolstering the inhibitory control of GSK3 is an important component of the therapeutic actions of drugs used to treat mood disorders and that GSK3 is a valid target for developing new therapeutic interventions.",
keywords = "glycogen synthase kinase-3, lithium, molecular and cellular neurobiology, mood disorders, neuropharmacology, signal transduction",
author = "Xiaohua Li and Jope, {Richard S}",
year = "2010",
month = "10",
day = "1",
doi = "10.1038/npp.2010.105",
language = "English",
volume = "35",
pages = "2143--2154",
journal = "Neuropsychopharmacology",
issn = "0893-133X",
publisher = "Nature Publishing Group",
number = "11",

}

TY - JOUR

T1 - Is glycogen synthase kinase-3 a central modulator in mood regulation

AU - Li, Xiaohua

AU - Jope, Richard S

PY - 2010/10/1

Y1 - 2010/10/1

N2 - Little is known regarding the mechanisms underlying the complex etiology of mood disorders, represented mainly by major depressive disorder and bipolar disorder. The 1996 discovery that lithium inhibits glycogen synthase kinase-3 (GSK3) raised the possibility that impaired inhibition of GSK3 is associated with mood disorders. This is now supported by evidence from animal biochemical, pharmacological, molecular, and behavioral studies and from human post-mortem brain, peripheral tissue, and genetic studies that are reviewed here. Mood disorders may result in part from impairments in mechanisms controlling the activity of GSK3 or GSK3-regulated functions, and disruptions of these regulating systems at different signaling sites may contribute to the heterogeneity of mood disorders. This substantial evidence supports the conclusion that bolstering the inhibitory control of GSK3 is an important component of the therapeutic actions of drugs used to treat mood disorders and that GSK3 is a valid target for developing new therapeutic interventions.

AB - Little is known regarding the mechanisms underlying the complex etiology of mood disorders, represented mainly by major depressive disorder and bipolar disorder. The 1996 discovery that lithium inhibits glycogen synthase kinase-3 (GSK3) raised the possibility that impaired inhibition of GSK3 is associated with mood disorders. This is now supported by evidence from animal biochemical, pharmacological, molecular, and behavioral studies and from human post-mortem brain, peripheral tissue, and genetic studies that are reviewed here. Mood disorders may result in part from impairments in mechanisms controlling the activity of GSK3 or GSK3-regulated functions, and disruptions of these regulating systems at different signaling sites may contribute to the heterogeneity of mood disorders. This substantial evidence supports the conclusion that bolstering the inhibitory control of GSK3 is an important component of the therapeutic actions of drugs used to treat mood disorders and that GSK3 is a valid target for developing new therapeutic interventions.

KW - glycogen synthase kinase-3

KW - lithium

KW - molecular and cellular neurobiology

KW - mood disorders

KW - neuropharmacology

KW - signal transduction

UR - http://www.scopus.com/inward/record.url?scp=78651312903&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78651312903&partnerID=8YFLogxK

U2 - 10.1038/npp.2010.105

DO - 10.1038/npp.2010.105

M3 - Article

VL - 35

SP - 2143

EP - 2154

JO - Neuropsychopharmacology

JF - Neuropsychopharmacology

SN - 0893-133X

IS - 11

ER -