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• W2015466061 abstract "<i>Backgroud:</i> Psychosis frequently occurs in Alzheimer’s disease (AD), being associated with more severe cognitive decline, but the underlying mechanisms are unknown. <i>Objective:</i> To investigate the effect of centrally administered β-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. <i>Methods:</i> Mice were intracerebroventricularly injected with β-amyloid (25–35), and after 1 week they were tested in the passive avoidance, spontaneous alternation and locomotor tasks. <i>Results:</i> Besides impaired performance in inhibitory avoidance and spontaneous alternation tasks, β-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. <i>Conclusion:</i> These results are compatible with the hypothesis that β-amyloid peptide may predispose to psychotic symptoms of AD by increasing sensitivity of the dopaminergic system, possibly related to a decreased adenosinergic inhibitory tone." @default.
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• W2015466061 date "2004-01-01" @default.
• W2015466061 modified "2023-10-14" @default.
• W2015466061 title "β-Amyloid Treatment Sensitizes Mice to Amphetamine-Induced Locomotion but Reduces Response to Caffeine" @default.
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• W2015466061 doi "https://doi.org/10.1159/000076668" @default.
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