title: Spatial deficits in a mouse model of Parkinson disease.
abstract: BACKGROUND
  Accumulating evidence in humans demonstrated that visuo-spatial deficits are the most consistently reported cognitive abnormalities in Parkinson disease (PD). These deficits have been generally attributed to cortical dopamine degeneration. However, more recent evidence suggests that dopamine loss in the striatum is responsible for the visuo-spatial abnormalities in PD. Studies based on animal models of PD did not specifically address this question.
  
  
  OBJECTIVE
  Thus, the first goal of this study was to analyze the role of dopamine within the dorsal striatum in spatial memory. We tested bilateral 6-OHDA striatal lesioned CD1 mice in an object-place association spatial task. Furthermore, to see whether the effects were selective for spatial information, we measured how the 6-OHDA-lesioned animals responded to a non-spatial change and learned in the one-trial inhibitory avoidance task.
  
  
  RESULTS
  The results demonstrated that bilateral (approximately 75%) dopamine depletion of the striatum impaired spatial change discrimination. On the contrary, no effect of the lesion was observed on non-spatial novelty detection or on passive avoidance learning.
  
  
  CONCLUSIONS
  These results confirm that dopamine depletion is accompanied by cognitive deficits and demonstrate that striatal dopamine dysfunction is sufficient to induce spatial information processing deficits.
authors.affiliation: Dipartimento di Genetica e Biologia Molecolare C Darwin, Università degli Studi di Roma La Sapienza, Piazzale Aldo Moro, 5, Rome, Italy. elvira.deleonibus@uniroma1.it
authors.forename: Elvira
authors.initials: E
authors.lastname: De Leonibus
authors.forename: Tiziana
authors.initials: T
authors.lastname: Pascucci
authors.forename: Sebastien
authors.initials: S
authors.lastname: Lopez
authors.forename: Alberto
authors.initials: A
authors.lastname: Oliverio
authors.forename: Marianne
authors.initials: M
authors.lastname: Amalric
authors.forename: Andrea
authors.initials: A
authors.lastname: Mele
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D021461:Animals, Outbred Strains; D001362:Avoidance Learning / Q000187:drug effects / Q000502:physiology; D001522:Behavior, Animal / Q000187:drug effects* / Q000502:physiology*; D003072:Cognition Disorders / Q000139:chemically induced / Q000503:physiopathology; D003627:Data Interpretation, Statistical; D004195:Disease Models, Animal; D004298:Dopamine / Q000032:analysis / Q000172:deficiency; D005106:Exploratory Behavior / Q000187:drug effects / Q000502:physiology; D006185:Habituation, Psychophysiologic / Q000187:drug effects / Q000502:physiology; D007150:Immunohistochemistry; D051379:Mice; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D009638:Norepinephrine / Q000032:analysis; D009714:Nucleus Accumbens / Q000737:chemistry / Q000187:drug effects / Q000473:pathology; D016627:Oxidopamine / Q000008:administration & dosage / Q000633:toxicity; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000503:physiopathology*; D015203:Reproducibility of Results; D013028:Space Perception / Q000187:drug effects / Q000502:physiology; D013037:Spatial Behavior / Q000187:drug effects / Q000502:physiology*; D013565:Sympatholytics / Q000008:administration & dosage / Q000633:toxicity; D013997:Time Factors
chemical_list: D013565:Sympatholytics; D016627:Oxidopamine; D004298:Dopamine; D009638:Norepinephrine