Altered emotionality leads to increased pain tolerance in amyloid β (Aβ1–40) peptide-treated mice
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- 作者：Fabrí ; cio A. Pamplona ; Pablo P ; olfo ; Filipe S. Duarte ; Reinaldo N. Takahashi ; Rui D.S. Prediger
- 关键词：Alzheimer's disease ; Beta-amyloid ; Pain ; Emotionality ; Cognition ; Mice
- 刊名：Behavioural Brain Research
- 出版年：2010
- 出版时间：1 September 2010
- 年：2010
- 卷：212
- 期：1
- 页码：96-102
- 全文大小：523 K
文摘
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the decline in cognitive functions, but it is also related to emotional disturbances. Since pain experience results from a complex integration of sensory, cognitive and affective processes, it is not surprising that AD patients display a distinct pattern of pain responsivity. We evaluated whether mice treated with amyloid β (Aβ) peptide—thought to be critical in the pathogenesis of AD—exhibit altered pain responses and its relation to altered emotionality. Mice received a single i.c.v. injection of vehicle (PBS) or Aβ fragment (1–40) (400 pmol/mice) and after 30 days, they were evaluated in tests of pain (hotplate, footshock-sensitivity), learning/memory (water-maze), emotionality (elevated plus-maze, forced swim) and locomotion (open-field). Aβ(1–40)-treated mice presented similar latencies to the control group in the hotplate test and similar nociceptive flinch threshold in the footshock-sensitivity test. However, they presented an increased jump threshold in footshock-sensitivity, suggesting increased pain tolerance. Altered emotionality was observed in the elevated plus-maze (EPM) and forced-swim tests (FST), suggesting anxiogenic-like and depressive-like states, respectively. A multifactorial principal component analysis (PCA) revealed that jump threshold of the footshock-sensitivity test falls within ‘Emotionality’ and ‘Pain’, showing moderate correlation with each one of the components of behavior. Acute treatment with the antidepressant desipramine (10 mg/kg, i.p.) reduced the jump threshold (i.e. pain tolerance) and time of immobility in FST (i.e. depressive-like state). Flinch threshold (i.e. pain sensitivity), locomotion and anxiety were not altered with desipramine treatment. These results suggest that Aβ(1–40) peptide increases pain tolerance, but not pain sensitivity in mice, which seems to be linked to alterations in cognitive/emotional components of pain processing.