title: Beta-amyloid treatment sensitizes mice to amphetamine-induced locomotion but reduces response to caffeine.
abstract: BACKGROUND
  Psychosis frequently occurs in Alzheimer's disease (AD), being associated with more severe cognitive decline, but the underlying mechanisms are unknown.
  
  
  OBJECTIVE
  To investigate the effect of centrally administered beta-amyloid peptide, a model for AD, in the locomotor response to amphetamine, caffeine and MK-801, which are psychoactive drugs related to neurochemical changes occurring in psychosis.
  
  
  METHODS
  Mice were intracerebroventricularly injected with beta-amyloid (25-35), and after 1 week they were tested in the passive avoidance, spontaneous alternation and locomotor tasks.
  
  
  RESULTS
  Besides impaired performance in inhibitory avoidance and spontaneous alternation tasks, beta-amyloid-treated mice showed increased spontaneous locomotion, augmented response to amphetamine (1.5 mg/kg), blunted response to caffeine (30 mg/kg) and no difference in MK-801 (0.25 mg/kg)-induced locomotor activation when compared to its respective control.
  
  
  CONCLUSIONS
  These results are compatible with the hypothesis that beta-amyloid peptide may predispose to psychotic symptoms of AD by increasing sensitivity of the dopaminergic system, possibly related to a decreased adenosinergic inhibitory tone.
authors.affiliation: Departamento de Bioquímica, Instituto de Ciencias Basicas da Saude, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil. oscar.dalligna@ufrgs.br
authors.forename: Oscar P
authors.initials: OP
authors.lastname: Dall'Igna
authors.forename: Anselmo
authors.initials: A
authors.lastname: Hoffmann
authors.forename: Adriana L
authors.initials: AL
authors.lastname: da Silva
authors.forename: Diogo O
authors.initials: DO
authors.lastname: Souza
authors.forename: Diogo R
authors.initials: DR
authors.lastname: Lara
mesh_terms: D000241:Adenosine / Q000378:metabolism; D018663:Adrenergic Agents / Q000494:pharmacology*; D000544:Alzheimer Disease / Q000150:complications / Q000503:physiopathology; D000661:Amphetamine / Q000494:pharmacology*; D016229:Amyloid beta-Peptides / Q000008:administration & dosage*; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002110:Caffeine / Q000494:pharmacology*; D000697:Central Nervous System Stimulants / Q000494:pharmacology; D004195:Disease Models, Animal; D016291:Dizocilpine Maleate / Q000494:pharmacology; D004298:Dopamine / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005973:Glutamine / Q000187:drug effects / Q000378:metabolism; D007276:Injections, Intraventricular; D008297:Male; D051379:Mice; D009043:Motor Activity / Q000187:drug effects*; D011618:Psychotic Disorders / Q000209:etiology / Q000503:physiopathology
chemical_list: D018663:Adrenergic Agents; D016229:Amyloid beta-Peptides; D000697:Central Nervous System Stimulants; D018691:Excitatory Amino Acid Antagonists; D005973:Glutamine; D002110:Caffeine; D016291:Dizocilpine Maleate; D000661:Amphetamine; D000241:Adenosine; D004298:Dopamine