Remodeling of neuronal networks by stress

Front Biosci. 2006 Sep 1;11:2746-58. doi: 10.2741/2004.

Abstract

Stress can be a threat to the physiological and psychological integrity of an individual and may result in psychic and behavioral changes. The stress response is mediated through in-concert activity of many brain areas and there is experimental evidence that stress induces structural changes in neuronal networks, in particular in the hippocampus, the prefrontal cortex and the amygdala. Within the hippocampal formation, stress exposure results in remodeling of dendrites of the CA3 pyramidal neurons and in reduced numbers of synapses on these neurons. Furthermore, stress inhibits adult neurogenesis in the dentate gyrus and appears to modulate the GABAergic system. In the prefrontal cortex, repeated exposure to stress causes dendritic retraction and loss of spines in pyramidal neurons whereas in the amygdala stress can elicit dendritic hypertrophy. These microscopically detectable changes in neuronal structures indicate the reorganization of neuronal networks. Moreover, molecular studies show that stress modulates expression of genes involved in neuronal differentiation and/or structural remodeling. Since a wealth of data documents the adverse effects of stress on emotions and cognition these alterations are commonly interpreted as the deleterious effect of chronic stress on the central nervous system. However, it is also possible that at least part of these changes reflect adaptive responses, as the network system rearranges its connections in order to cope with the changing requirements from the internal or external environment.

Publication types

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

MeSH terms

  • Cell Differentiation
  • Dendrites
  • Gene Expression Regulation
  • Glucocorticoids / pharmacology
  • Hippocampus / pathology*
  • Humans
  • Hypertrophy
  • Nerve Net*
  • Neuronal Plasticity
  • Neurons
  • Receptors, GABA / physiology
  • Stress, Psychological*

Substances

  • Glucocorticoids
  • Receptors, GABA