Stress-induced, glucocorticoid-dependent strengthening of glutamatergic synaptic transmission in midbrain dopamine neurons

Neurosci Lett. 2009 Mar 20;452(3):273-6. doi: 10.1016/j.neulet.2009.01.070. Epub 2009 Feb 3.

Abstract

Stress facilitates development of addictive behaviors in part by stress-induced increase in the strength of glutamatergic synapses at dopamine (DA) neurons within the ventral tegmental area (VTA). Here, we further demonstrate that this stress-induced synaptic adaptation is glucocorticoid-dependent and is progressively developed. Activation of glucocorticoid receptors (GRs) either by in vivo injection of dexamethasone (Dex) or incubation of the VTA slice with Dex potentiate the synaptic strength of glutamatergic synapses at VTA DA neurons, whereas preventing the activation of GRs by Ru486 abolishes this effect. These results suggest that the VTA GRs play a critical role in stress-induced cellular adaptations.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Dexamethasone / pharmacology
  • Dopamine / metabolism*
  • Excitatory Postsynaptic Potentials / drug effects
  • Glucocorticoids / antagonists & inhibitors
  • Glucocorticoids / metabolism*
  • Glucocorticoids / pharmacology
  • Glutamic Acid / metabolism*
  • Hormone Antagonists / pharmacology
  • In Vitro Techniques
  • Male
  • Mifepristone / pharmacology
  • Neurons / physiology
  • Patch-Clamp Techniques
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Glucocorticoid / metabolism
  • Stress, Psychological / physiopathology*
  • Synaptic Transmission*
  • Time Factors
  • Ventral Tegmental Area / physiopathology*

Substances

  • Glucocorticoids
  • Hormone Antagonists
  • Receptors, Glucocorticoid
  • Mifepristone
  • Glutamic Acid
  • Dexamethasone
  • Dopamine