Electroacupuncture Potentiates Cannabinoid Receptor-Mediated Descending Inhibitory Control in a Mouse Model of Knee Osteoarthritis
Autor: | Hui Lin Pan, Fang Gao, Man Li, Wei He, Xiang Hong Jing, Xiao Cui Yuan, Cai Hua Wu, Chuan You Lin, He Zhu, Bin Zhou, Li Ze Xiong, Hong Ping Li, Hong Chun Xiang, Bing Zhu, Qiang Wang |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
AM251
Cannabinoid receptor Electroacupuncture medicine.medical_treatment diffuse noxious inhibitory controls (DNIC) Osteoarthritis Pharmacology lcsh:RC321-571 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine 030202 anesthesiology medicine knee osteoarthritis (KOA) electroacupuncture analgesia endocannabinoids Molecular Biology lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry Original Research business.industry Diffuse noxious inhibitory control Chronic pain medicine.disease Endocannabinoid system Cannabinoid business chronic pain 030217 neurology & neurosurgery medicine.drug Neuroscience |
Zdroj: | Frontiers in Molecular Neuroscience, Vol 11 (2018) Frontiers in Molecular Neuroscience |
ISSN: | 1662-5099 |
Popis: | Knee osteoarthritis (KOA) is a highly prevalent, chronic joint disorder, which can lead to chronic pain. Although electroacupuncture (EA) is effective in relieving chronic pain in the clinic, the involved mechanisms remain unclear. Reduced diffuse noxius inhibitory controls (DNIC) function is associated with chronic pain and may be related to the action of endocannabinoids. In the present study, we determined whether EA may potentiate cannabinoid receptor-mediated descending inhibitory control and inhibit chronic pain in a mouse model of KOA. We found that the optimized parameters of EA inhibiting chronic pain were the low frequency and high intensity (2 Hz + 1 mA). EA reversed the reduced expression of CB1 receptors and the 2-arachidonoylglycerol (2-AG) level in the midbrain in chronic pain. Microinjection of the CB1 receptor antagonist AM251 into the ventrolateral periaqueductal gray (vlPAG) can reversed the EA effect on pain hypersensitivity and DNIC function. In addition, CB1 receptors on GABAergic but not glutamatergic neurons are involved in the EA effect on DNIC function and descending inhibitory control of 5-HT in the medulla, thus inhibiting chronic pain. Our data suggest that endocannabinoid (2-AG)-CB1R-GABA-5-HT may be a novel signaling pathway involved in the effect of EA improving DNIC function and inhibiting chronic pain. |
Databáze: | OpenAIRE |
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