title: Neuropeptide Y (NPY) suppresses yohimbine-induced reinstatement of alcohol seeking.
abstract: BACKGROUND
  Reinstatement of responding to a previously alcohol-associated lever following extinction is an established model of relapse-like behavior and can be triggered by stress exposure. Here, we examined whether neuropeptide Y (NPY), an endogenous anti-stress mediator, blocks reinstatement of alcohol-seeking induced by the pharmacological stressor yohimbine.
  
  
  METHODS
  NPY [5.0 or 10.0 mug/rat, intracerebroventricularly (ICV)] dose-dependently blocked the reinstatement of alcohol seeking induced by yohimbine (1.25 mg/kg, i.p.) but failed to significantly suppress the maintenance of alcohol self-administration. We then used c-fos expression mapping to examine neuronal activation following treatment with yohimbine or NPY alone or yohimbine following NPY pre-treatment.
  
  
  CONCLUSIONS
  The analysis was focused on a network of structures previously implicated in yohimbine-induced reinstatement, comprised of central (CeA) and basolateral (BLA) amygdala and the shell of the nucleus accumbens (Nc AccS). Within this network, both yohimbine and NPY potently induced neuronal activation, and their effects were additive, presumably indicating activation of excitatory and inhibitory neuronal populations, respectively.
  
  
  CONCLUSIONS
  These results suggest that NPY selectively suppresses relapse to alcohol seeking induced by stressful events and support the NPY system as an attractive target for the treatment of alcohol addiction.
authors.affiliation: Laboratory of Clinical and Translational Studies, National Institute of Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH), 10 Center Dr. 1/5330, Bethesda, MD 20892-1108, USA.
authors.forename: Andrea
authors.initials: A
authors.lastname: Cippitelli
authors.forename: Ruslan
authors.initials: R
authors.lastname: Damadzic
authors.forename: Anita C
authors.initials: AC
authors.lastname: Hansson
authors.forename: Erick
authors.initials: E
authors.lastname: Singley
authors.forename: Wolfgang H
authors.initials: WH
authors.lastname: Sommer
authors.forename: Robert
authors.initials: R
authors.lastname: Eskay
authors.forename: Annika
authors.initials: A
authors.lastname: Thorsell
authors.forename: Markus
authors.initials: M
authors.lastname: Heilig
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology*; D000428:Alcohol Drinking / Q000378:metabolism / Q000523:psychology*; D000818:Animals; D016739:Behavior, Addictive; D001522:Behavior, Animal; D003216:Conditioning, Operant / Q000187:drug effects; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D008297:Male; D009478:Neuropeptide Y / Q000494:pharmacology / Q000502:physiology*; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D012055:Reinforcement Schedule; D012646:Self Administration; D015016:Yohimbine / Q000494:pharmacology*
chemical_list: D000317:Adrenergic alpha-Antagonists; D009478:Neuropeptide Y; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger; D015016:Yohimbine; D003346:Corticotropin-Releasing Hormone