| Autor: |
Merlo, Sara, Costa, Lara, Chiechio, Santina, Busceti, Carla Letizia, Ciranna, Lucia, Santangelo, Rosa, Sortino, Maria Angela, Fornai, Francesco, Nicoletti, Ferdinando, Copani, Agata |
| Předmět: |
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| Zdroj: |
Journal of Alzheimer's Disease; 2023, Vol. 96 Issue 1, p77-91, 15p |
| Abstrakt: |
Background: The effects of Alzheimer's disease (AD) pathology on the experience of pain are poorly understood. Objective: To understand the pathophysiological mechanisms underlying pain sensory transmission in the transgenic mouse model of AD, CRND8. Methods: We explored AD-related pathology in the spinal cord and dorsal root ganglia of 18-week-old female CRND8 mice. We assessed nociceptive responses to both acute heat stimuli and persistent inflammatory pain in CRND8 mice and non-transgenic (non-Tg) littermates. In addition, we searched for differences in biochemical correlates of inflammatory pain between CRND8 and non-Tg mice. Finally, we investigated the excitability of dorsal horn noc iceptive neurons in spinal cord slices from CRND8 and non-Tg mice. Results: We demonstrated the presence of intracellular AD-like pathology in the spinal cord and in the dorsal root ganglia nociceptive sensory neurons of CRND8 mice. We found that CRND8 mice had a reduced susceptibility to acute noxious heat stimuli and an increased sensitivity to tonic inflammatory pain. Tonic inflammatory pain correlated with a lack of induction of pro-opiomelanocortin in the spinal cord of CRND8 mice as compared to non-Tg mice. Electrophysiological recording in acute spinal cord slice preparations indicated an increased probability of glutamate release at the membrane of dorsal horn nociceptive neurons in CRND8 mice. Conclusion: This study suggests that an increased thermal tolerance and a facilitation of nociception by peripheral inflammation can coexist in AD. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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