title: Decreased prefrontal cortex dopamine activity following adolescent social defeat in male rats: role of dopamine D2 receptors.
abstract: BACKGROUND
  Adverse social experience in adolescence causes reduced medial prefrontal cortex (mPFC) dopamine (DA) and associated behavioral deficits in early adulthood.
  
  
  OBJECTIVE
  This study aims to determine whether mPFC DA hypofunction following social stress is specific to adolescent experience and if this results from stress-induced DA D2 receptor activation.
  
  
  METHODS
  Male rats exposed to repeated social defeat during adolescence or adulthood had mPFC DA activity sampled 17 days later. Separate experiments used freely moving microdialysis to measure mPFC DA release in response to adolescent defeat exposure. At P40, 49 and 56 mPFC DA turnover was assessed to identify when DA activity decreased in relation to the adolescent defeat experience. Finally, nondefeated adolescent rats received repeated intra-mPFC infusions of the D2 receptor agonist quinpirole, while another adolescent group received intra-mPFC infusions of the D2 antagonist amisulpride before defeat exposure.
  
  
  RESULTS
  Long-term decreases or increases in mPFC DA turnover were observed following adolescent or adult defeat, respectively. Adolescent defeat exposure elicits sustained increases in mPFC DA release, and DA turnover remains elevated beyond the stress experience before declining to levels below normal at P56. Activation of mPFC D2 receptors in nondefeated adolescents decreases DA activity in a similar manner to that caused by adolescent defeat, while defeat-induced reductions in mPFC DA activity are prevented by D2 receptor blockade.
  
  
  CONCLUSIONS
  Both the developing and mature PFC DA systems are vulnerable to social stress, but only adolescent defeat causes DA hypofunction. This appears to result in part from stress-induced activation of mPFC D2 autoreceptors.
authors.affiliation: Center for Brain and Behavior Research, Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, 414 E Clark St, Vermillion, SD, 57069, USA, Mick.Watt@usd.edu.
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Watt
authors.forename: Christina L
authors.initials: CL
authors.lastname: Roberts
authors.forename: Jamie L
authors.initials: JL
authors.lastname: Scholl
authors.forename: Danielle L
authors.initials: DL
authors.lastname: Meyer
authors.forename: Leah C
authors.initials: LC
authors.lastname: Miiller
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Barr
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Novick
authors.forename: Kenneth J
authors.initials: KJ
authors.lastname: Renner
authors.forename: Gina L
authors.initials: GL
authors.lastname: Forster
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000077582:Amisulpride; D000818:Animals; D002408:Catheters, Indwelling; D004291:Dominance-Subordination; D004298:Dopamine / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology; D065127:Dopamine D2 Receptor Antagonists / Q000494:pharmacology; D008297:Male; D017551:Microdialysis; D017397:Prefrontal Cortex / Q000187:drug effects / Q000254:growth & development* / Q000503:physiopathology*; D019257:Quinpirole / Q000494:pharmacology; D017207:Rats, Sprague-Dawley; D017448:Receptors, Dopamine D2 / Q000819:agonists / Q000378:metabolism*; D013315:Stress, Psychological / Q000188:drug therapy / Q000503:physiopathology*; D013469:Sulpiride / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D018491:Dopamine Agonists; D065127:Dopamine D2 Receptor Antagonists; D017448:Receptors, Dopamine D2; D015102:3,4-Dihydroxyphenylacetic Acid; D019257:Quinpirole; D013469:Sulpiride; D000077582:Amisulpride; D004298:Dopamine