期刊
PAIN
卷 163, 期 11, 页码 2138-2153出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/j.pain.0000000000002648
关键词
Alzheimer disease; Chronic pain; ACC; Hypesthesia; Dendritic spine
资金
- Chinese National Natural Science Foundation of China [62127810, 31701217, 81970418]
- Shanghai Key Laboratory of Health Identification and Assessment [21DZ2271000]
Research indicates that abnormal pain sensitivity in Alzheimer's disease modeling mice is closely related to changes in neuronal activity and dendritic spine loss in ACC pyramidal neurons, highlighting the crucial role of dendritic spine density in pain processing.
Chronic pain is highly prevalent. Individuals with cognitive disorders such as Alzheimer disease are a susceptible population in which pain is frequently difficult to diagnosis. It is still unclear whether the pathological changes in patients with Alzheimer disease will affect pain processing. Here, we leverage animal behavior, neural activity recording, optogenetics, chemogenetics, and Alzheimer disease modeling to examine the contribution of the anterior cingulate cortex (ACC) neurons to pain response. The 5x familial Alzheimer disease mice show alleviated mechanical allodynia which can be regained by the genetic activation of ACC excitatory neurons. Furthermore, the lower peak neuronal excitation, delayed response initiation, as well as the dendritic spine reduction of ACC pyramidal neurons in 5xfamilial Alzheimer disease mice can be mimicked by Rac1 or actin polymerization inhibitor in wild-type (WT) mice. These findings indicate that abnormal of pain sensitivity in Alzheimer disease modeling mice is closely related to the variation of neuronal activity and dendritic spine loss in ACC pyramidal neurons, suggesting the crucial role of dendritic spine density in pain processing.
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