title: Chronic stress causes amygdala hyperexcitability in rodents.
abstract: BACKGROUND
  Chronic stress is a major health concern, often leading to depression, anxiety, or when severe enough, posttraumatic stress disorder. While many studies demonstrate that the amygdala is hyperresponsive in patients with these disorders, the cellular neurophysiological effects of chronic stress on the systems that underlie psychiatric disorders, such as the amygdala, are relatively unknown.
  
  
  METHODS
  In this study, we examined the effects of chronic stress on the activity and excitability of amygdala neurons in vivo in rats. We used in vivo intracellular recordings from single neurons of the lateral amygdala (LAT) to measure neuronal properties and determine the cellular mechanism for the effects of chronic stress on LAT neurons.
  
  
  RESULTS
  We found a mechanism for the effects of chronic stress on amygdala activity, specifically that chronic stress increased excitability of LAT pyramidal neurons recorded in vivo. This hyperexcitability was caused by a reduction of a regulatory influence during action potential firing, facilitating LAT neuronal activity. The effects of stress on excitability were occluded by agents that block calcium-activated potassium channels and reversed by pharmacological enhancement of calcium-activated potassium channels.
  
  
  CONCLUSIONS
  These data demonstrate a specific channelopathy that occurs in the amygdala after chronic stress. This enhanced excitability of amygdala neurons after chronic stress may explain the observed hyperresponsiveness of the amygdala in patients with posttraumatic stress disorder and may facilitate the emergence of depression or anxiety in other patients.
authors.affiliation: Department of Cellular and Molecular Pharmacology, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA. jeremy.rosenkranz@rosalindfranklin.edu
authors.forename: J Amiel
authors.initials: JA
authors.lastname: Rosenkranz
authors.forename: Emily R
authors.initials: ER
authors.lastname: Venheim
authors.forename: Mallika
authors.initials: M
authors.lastname: Padival
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000311:Adrenal Glands / Q000503:physiopathology; D000679:Amygdala / Q000187:drug effects / Q000503:physiopathology*; D000818:Animals; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002908:Chronic Disease; D008297:Male; D018782:Maze Learning / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024681:Potassium Channels, Calcium-Activated / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013267:Stilbenes / Q000494:pharmacology; D013315:Stress, Psychological / Q000503:physiopathology*
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D026902:Potassium Channel Blockers; D024681:Potassium Channels, Calcium-Activated; D013267:Stilbenes; C022306:4,4'-dinitro-2,2'-stilbenedisulfonic acid