title: Role of IL-1 in poststroke depressive-like behavior in mice.
abstract: BACKGROUND
  Poststroke depression (PSD) leads to impaired functional recovery and increased mortality, yet physiological mechanisms are unknown. The present study investigates the roles of glucocorticoids and interleukin-1 (IL-1) in poststroke anhedonia.
  
  
  METHODS
  Adult male mice underwent middle cerebral artery occlusion (MCAO), and were recovered 7 days. Mice were treated with metyrapone (100 mg/kg intraperitoneally), mifepristone (50 mg/kg subcutaneously), or vehicle injections on reperfusion days 4-7. A separate cohort of mice was implanted with cannulae and was administered IL-1 receptor antagonist (IL-1ra) or vehicle (6 microg intracerebroventricularly) on reperfusion days 6 and 7. After the final injection or infusion, sucrose consumption was recorded for 6 hours.
  
  
  RESULTS
  Mice in the sham-treated group consumed significantly more sucrose solution than water, whereas MCAO-treated mice consumed similar amounts of each, suggesting anhedonia among MCAO-treated mice. A separate experiment assessed whether stroke-induced increases in corticosteroids or IL-1 contribute to anhedonia. Only IL-1ra restored sucrose consumption in MCAO-treated mice. Vehicle-MCAO-treated mice drank significantly less sucrose solution than did both IL-1ra and vehicle-sham treatment groups, whereas IL-1ra-MCAO-treated mice drank similar amounts to both sham-treated groups.
  
  
  CONCLUSIONS
  Poststroke anhedonia, a symptom of depression in human beings, can be reproduced in a mouse model of stroke and appears to involve altered IL-1 transmission in the brain.
authors.affiliation: Department of Psychology, The Ohio State University, Columbus, Ohio 43210-1287, USA.
authors.forename: Tara K S
authors.initials: TK
authors.lastname: Craft
authors.forename: A Courtney
authors.initials: AC
authors.lastname: DeVries
mesh_terms: D000818:Animals; D000963:Antimetabolites / Q000008:administration & dosage / Q000494:pharmacology; D003866:Depressive Disorder / Q000209:etiology / Q000503:physiopathology* / Q000523:psychology*; D004327:Drinking Behavior / Q000187:drug effects; D005938:Glucocorticoids / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D006727:Hormone Antagonists / Q000008:administration & dosage / Q000494:pharmacology; D020244:Infarction, Middle Cerebral Artery / Q000473:pathology / Q000503:physiopathology / Q000523:psychology; D007276:Injections, Intraventricular; D007375:Interleukin-1 / Q000502:physiology*; D008297:Male; D008797:Metyrapone / Q000008:administration & dosage / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D015735:Mifepristone / Q000008:administration & dosage / Q000494:pharmacology; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D020521:Stroke / Q000150:complications / Q000503:physiopathology* / Q000523:psychology*; D013395:Sucrose
chemical_list: D000963:Antimetabolites; D005938:Glucocorticoids; D006727:Hormone Antagonists; D007375:Interleukin-1; D011965:Receptors, Glucocorticoid; D017472:Receptors, Interleukin-1; D015735:Mifepristone; D013395:Sucrose; D008797:Metyrapone