Second messenger/signal transduction pathways in major mood disorders: Moving from membrane to mechanism of action, part II: Bipolar disorder

Mark J. Niciu, Dawn F. Ionescu, Daniel C. Mathews, Erica M. Richards, Carlos A. Zarate

Research output: Contribution to journalReview articlepeer-review

Abstract

In this second of two articles on second messenger/signal transduction cascades in major mood disorders, we will review the evidence in support of intracellular dysfunction and its rectification in the etiopathogenesis and treatment of bipolar disorder (BD). The importance of these cascades is highlighted by lithium's (the gold standard in BD psychopharmacology) ability to inhibit multiple critical loci in second messenger/signal transduction cascades including protein kinase C (involved in the IP3/PIP2 pathway) and GSK-3β (canonically identified in the Wnt/Fz/Dvl/GSK-3β cascade). As a result, and like major depressive disorder (MDD), more recent pathophysiological studies and rational therapeutic targets have been directed at these and other intracellular mediators. Even in the past decade, intracellular dysfunction in numerous neuroprotective/apoptotic cascades appears important in the pathophysiology and may be a future target for pharmacological interventions of BD.

Original languageEnglish (US)
Pages (from-to)242-251
Number of pages10
JournalCNS spectrums
Volume18
Issue number5
DOIs
StatePublished - Oct 2013
Externally publishedYes

Keywords

  • Bipolar disorder
  • intracellular cascades
  • lithium
  • mood stabilizers
  • second messenger
  • signal transduction

ASJC Scopus subject areas

  • Clinical Neurology
  • Psychiatry and Mental health

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