Inhibition of the central extended amygdala by loud noise and restraint stress

Eur J Neurosci. 2005 Jan;21(2):441-54. doi: 10.1111/j.1460-9568.2005.03865.x.


It is well established that the central nucleus of the amygdala (CEA) is involved in responses to stress, fear and anxiety. Many studies have used c-fos expression to map the brain's response to processive stress, but curiously the CEA generally is not highly activated. We have previously shown that exposure to a novel vs. home environment reduces amphetamine-induced activation of the lateral CEA (CEAl) and the oval nucleus of the bed nucleus of the stria terminalis (BSTov). This is consistent with the idea that processive stress inhibits neurons in these nuclei. We have tested this hypothesis by exposing rats to noise, at a range of intensities from non-stressful to stressful, or to restraint conditions, immediately after a remote injection of amphetamine, 2 mg/kg i.p., or interleukin-1beta (IL-1beta) 0.5 microg/kg i.p. (used to obtain a level of c-fos mRNA against which to measure inhibition). In keeping with our hypothesis, amphetamine- or IL-1beta-induced c-fos and zif-268 mRNA were significantly decreased in the CEAl and BSTov under conditions of loud noise or restraint stress compared with control conditions. This inhibition does not require a stress-induced rise in corticosterone because data were similar in animals that had been adrenalectomized with a low-dose corticosterone replacement. As both the CEAl and BSTov are highly gamma-aminobutyric acid (GABA) -ergic and project to the medial CEA (CEAm), their inhibition potentially causes an increased input to the CEAm. As the CEAm is a major output nucleus of the amygdala, this could have important consequences within the neural circuitry controlling responses to processive stress.

Publication types

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

MeSH terms

  • Acoustic Stimulation / methods
  • Amphetamine / pharmacology
  • Amygdala / drug effects
  • Amygdala / metabolism
  • Amygdala / physiopathology
  • Amygdala / radiation effects*
  • Analysis of Variance
  • Animals
  • Behavior, Animal / drug effects
  • Behavior, Animal / radiation effects
  • Central Nervous System Stimulants / pharmacology
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Dose-Response Relationship, Radiation
  • Early Growth Response Protein 1
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / radiation effects
  • Immediate-Early Proteins / genetics
  • Immediate-Early Proteins / metabolism
  • In Situ Hybridization / methods
  • Male
  • Models, Biological
  • Neural Inhibition / drug effects
  • Neural Inhibition / physiology*
  • Neural Inhibition / radiation effects
  • Noise*
  • Paraventricular Hypothalamic Nucleus / drug effects
  • Paraventricular Hypothalamic Nucleus / metabolism
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-fos / metabolism
  • RNA, Messenger / biosynthesis
  • Rats
  • Rats, Sprague-Dawley
  • Restraint, Physical / methods
  • Reverse Transcriptase Polymerase Chain Reaction / methods
  • Stress, Physiological / metabolism
  • Stress, Physiological / physiopathology*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism


  • Central Nervous System Stimulants
  • DNA-Binding Proteins
  • Early Growth Response Protein 1
  • Egr1 protein, rat
  • Immediate-Early Proteins
  • Proto-Oncogene Proteins c-fos
  • RNA, Messenger
  • Transcription Factors
  • Amphetamine