title: Hyperactivity in the Gunn rat model of neonatal jaundice: age-related attenuation and emergence of gait deficits.
abstract: BACKGROUND
  Neonatal jaundice resulting from elevated unconjugated bilirubin occurs in 60-80% of newborn infants. Although mild jaundice is generally considered harmless, little is known about its long-term consequences. Recent studies have linked mild bilirubin-induced neurological dysfunction (BIND) with a range of neurological syndromes, including attention-deficit hyperactivity disorder. The goal of this study was to measure BIND across the lifespan in the Gunn rat model of BIND.
  
  
  METHODS
  Using a sensitive force plate actometer, we measured locomotor activity and gait in jaundiced (jj) Gunn rats versus their nonjaundiced (Nj) littermates. Data were analyzed for young adult (3-4 mo), early middle-aged (9-10 mo), and late middle-aged (17-20 mo) male rats.
  
  
  RESULTS
  jj rats exhibited lower body weights at all ages and a hyperactivity that resolved at 17-20 mo of age. Increased propulsive force and gait velocity accompanied hyperactivity during locomotor bouts at 9-10 mo in jj rats. Stride length did not differ between the two groups at this age. Hyperactivity normalized, and gait deficits, including decreased stride length, propulsive force, and gait velocity, emerged in the 17-20-mo-old jj rats.
  
  
  CONCLUSIONS
  These results demonstrate that, in aging, hyperactivity decreases with the onset of gait deficits in the Gunn rat model of BIND.
authors.affiliation: Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas.
authors.forename: John A
authors.initials: JA
authors.lastname: Stanford
authors.affiliation: Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas.
authors.forename: Jeffrey M
authors.initials: JM
authors.lastname: Shuler
authors.affiliation: Department of Pharmacology and Toxicology, University of Kansas, Lawrence, Kansas.
authors.forename: Stephen C
authors.initials: SC
authors.lastname: Fowler
authors.affiliation: Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas.
authors.forename: Kimberly G
authors.initials: KG
authors.lastname: Stanford
authors.affiliation: Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas.
authors.forename: Delin
authors.initials: D
authors.lastname: Ma
authors.affiliation: The Ward Family Heart Center, Children's Mercy Hospital, Kansas City, Missouri.
authors.forename: Douglas C
authors.initials: DC
authors.lastname: Bittel
authors.affiliation: 1] Department of Neurology, Children's Mercy Hospital, Kansas City, Missouri [2] Departments of Neurology and Pediatrics, University of Kansas Medical Center, Kansas City, Kansas [3] Department of Pediatrics, University of Missouri-Kansas City, Kansas City, Missouri.
authors.forename: Jean-Baptiste
authors.initials: JB
authors.lastname: Le Pichon
authors.affiliation: 1] Department of Neurology, Children's Mercy Hospital, Kansas City, Missouri [2] Departments of Neurology and Pediatrics, University of Kansas Medical Center, Kansas City, Kansas [3] Department of Pediatrics, University of Missouri-Kansas City, Kansas City, Missouri.
authors.forename: Steven M
authors.initials: SM
authors.lastname: Shapiro
mesh_terms: D000367:Age Factors; D000818:Animals; D001663:Bilirubin / Q000097:blood; D020234:Gait Ataxia / Q000209:etiology*; D006948:Hyperkinesis / Q000209:etiology*; D007567:Jaundice, Neonatal / Q000150:complications*; D008124:Locomotion / Q000502:physiology; D008297:Male; D051381:Rats; D011911:Rats, Gunn
chemical_list: D001663:Bilirubin