Intracellular mechanisms of antidepressant drug action

Harv Rev Psychiatry. 2000 Oct;8(4):161-74.

Abstract

The action of antidepressant drugs on monoamines such as norepinephrine and serotonin has been described for three decades. However, more-recent research has looked beyond cell surface receptors to transductional cascades and gene expression. Antidepressant drug therapies seem to share several mechanisms involved in either activating the adenylyl cyclase-protein kinase A cascade or inhibiting the phospholipase C-protein kinase C mechanisms. These effects, ultimately, combine to regulate the expression of target genes. Several specific genes are known to be activated or inhibited by antidepressant therapies. Steady-state levels of mRNA for glucocorticoid and mineralocorticoid receptors, brain-derived neurotrophic factor and its receptor trkB, and preproenkephalin are enhanced, whereas those for corticotropin-releasing hormone, c-fos,N-methyl-D-aspartate receptor subunits, and nerve-growth factor 1A are reduced. New molecular genetic methods for identifying differentially expressed genes will aid in the development of targets for wholly new generations of antidepressant drug therapies.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Antidepressive Agents / pharmacology*
  • Drug Design
  • Gene Expression Regulation / drug effects*
  • Gene Expression Regulation / genetics
  • Humans
  • Models, Genetic
  • RNA, Messenger / drug effects
  • RNA, Messenger / metabolism
  • Second Messenger Systems / drug effects
  • Second Messenger Systems / genetics
  • Signal Transduction / drug effects*
  • Signal Transduction / genetics

Substances

  • Antidepressive Agents
  • RNA, Messenger