Stress-triggered activation of gene expression in catecholaminergic systems: dynamics of transcriptional events

Trends Neurosci. 2001 Feb;24(2):91-8. doi: 10.1016/s0166-2236(00)01687-8.

Abstract

Stress triggers important adaptive responses that enable an organism to cope with a changing environment. However, when prolonged or repeated, stress can be extremely harmful. The release of catecholamines is a key initial event in responses to stressors and is followed by an increase in the expression of genes that encode catecholamine-synthesizing enzymes. This process is mediated by transcriptional mechanisms in the adrenal medulla and the locus coeruleus. The persistence of transcriptional activation depends on the duration and repetition of the stress. Recent work has begun to identify the various transcription factors that are associated with brief or intermediate duration of a single or repeated stress. These studies suggest that dynamic interplay is involved in converting the transient increases in the rate of transcription into prolonged (potentially adaptive or maladaptive) changes in gene expression.

Publication types

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

MeSH terms

  • Adrenal Medulla / metabolism
  • Animals
  • Catecholamines / metabolism*
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Dopamine beta-Hydroxylase / metabolism
  • Gene Expression / physiology*
  • Humans
  • Locus Coeruleus / metabolism
  • Phenylethanolamine N-Methyltransferase / metabolism
  • Proto-Oncogene Proteins c-fos / metabolism
  • RNA, Messenger / metabolism
  • Stress, Physiological / metabolism*
  • Transcription Factors / metabolism*
  • Transcription, Genetic / physiology*
  • Tyrosine 3-Monooxygenase / metabolism

Substances

  • Catecholamines
  • Cyclic AMP Response Element-Binding Protein
  • Proto-Oncogene Proteins c-fos
  • RNA, Messenger
  • Transcription Factors
  • Tyrosine 3-Monooxygenase
  • Dopamine beta-Hydroxylase
  • Phenylethanolamine N-Methyltransferase