Amygdala Metabotropic Glutamate Receptor 1 Influences Synaptic Transmission to Participate in Fentanyl-Induced Hyperalgesia in Rats

The underlying mechanisms of opioid-induced hyperalgesia (OIH) remain unclear. Herein, we found that the protein expression of metabotropic glutamate receptor 1 (mGluR1) was significantly increased in the right but not in the left laterocapsular division of central nucleus of the amygdala (CeLC) in...

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Published in:Cellular and molecular neurobiology 2023-04, Vol.43 (3), p.1401-1412
Main Authors: Bai, Tianyu, Chen, Hengling, Hu, Wenwu, Liu, Jingtao, Lin, Xianguang, Chen, Su, Luo, Fang, Yang, Xiaofei, Chen, Jun, Li, Chenhong
Format: Article
Language:English
Subjects:
Amygdala
Amygdala - metabolism
Analgesics, Opioid - pharmacology
Animals
Biomedical and Life Sciences
Biomedicine
Brief Communication
Cell Biology
Excitatory postsynaptic potentials
Fentanyl
Glutamic acid receptors (metabotropic)
Hyperalgesia
Hyperalgesia - chemically induced
Microinjection
Neurobiology
Neurosciences
Pain perception
Rats
Rats, Sprague-Dawley
Receptors, Metabotropic Glutamate - metabolism
Synaptic Transmission
Therapeutic targets
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Summary:The underlying mechanisms of opioid-induced hyperalgesia (OIH) remain unclear. Herein, we found that the protein expression of metabotropic glutamate receptor 1 (mGluR1) was significantly increased in the right but not in the left laterocapsular division of central nucleus of the amygdala (CeLC) in OIH rats. In CeLC neurons, the frequency and the amplitude of mini-excitatory postsynaptic currents (mEPSCs) were significantly increased in fentanyl group which were decreased by acute application of a mGluR1 antagonist, A841720. Finally, the behavioral hypersensitivity could be reversed by A841720 microinjection into the right CeLC. These results show that the right CeLC mGluR1 is an important factor associated with OIH that enhances synaptic transmission and could be a potential drug target to alleviate fentanyl-induced hyperalgesia. Graphical Abstract
ISSN:0272-4340
1573-6830
DOI:10.1007/s10571-022-01248-x