1. A neural circuit for alcohol withdrawal-induced hyperalgesia in a nondependent state.
- Author
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Yang XL, Gao W, Dong WY, Zheng C, Wang S, Wei HR, Luo Y, Zhang Z, Chen Y, and Jin Y
- Subjects
- Animals, Mice, Disease Models, Animal, Gyrus Cinguli physiopathology, Male, Alcoholism complications, Neural Pathways, Mice, Inbred C57BL, CA1 Region, Hippocampal metabolism, CA1 Region, Hippocampal pathology, Glutamic Acid metabolism, Hyperalgesia etiology, Substance Withdrawal Syndrome, Ethanol adverse effects, Neurons metabolism
- Abstract
Alcohol use disorder is highly prevalent worldwide, with characteristically severe pain sensitivity during withdrawal. Here, we established a mouse model of hyperalgesia during ethanol withdrawal (EW) before addiction to investigate the window for onset and underlying mechanisms. Viral tracing with in vivo microendoscopic and two-photon calcium imaging identified a circuit pathway from dorsal hippocampal CA1 glutamatergic neurons (dCA1
Glu ) to anterior cingulate cortex glutamatergic neurons (ACCGlu ) activated in EW mice with hyperalgesia. Chemogenetic inhibition of this pathway can alleviate hyperalgesia in EW mice, whereas artificial activation recapitulates EW-induced hyperalgesia in naïve mice. These findings demonstrate that the dCA1Glu → ACCGlu neuronal pathway participates in driving EW-induced hyperalgesia before ethanol dependence in mice.- Published
- 2024
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