Objective: To explore the expression and distribution of μ-opioid receptors(MOR) in intracardiac ganglia(ICG) and the effect of its agonists on atrial fibrillation(AF). Methods: (1) The chemical anatomical characteristics of ICG in normal SD rats were studied by immunofluorescence single staining. The expression and distribution of MOR in ICG were detected by using immunofluorescence double staining, Western blot, and RT-PCR.(2) Forty male SD rats weighing 250-300 g were randomly divided into 5 groups: normal group, AF model group(AF group), solvent control group(AF-NS group), MOR-specific agonist endomorphin-2(EM2) drug group(AF-EM2 group) and DAMGO drug group(AF-DAMGO group). The AF model was established by tail vein injection of acetylcholine(Ach) and CaCl2, and drug intervention was given during modeling. The duration of AF before and after drug administration was monitored by collecting electrocardiograms. The protein and mRNA expression of MOR in ICG and connexin 43(CX43) in atrial tissue were detected by the method of Western blot and qRT-PCR. Results: (1) Peptide nerve fibers positive for substance P and calcitonin gene-related peptide were found in the ICG, along with parasympathetic neurons positive for acetylcholine transferase and sympathetic neurons positive for tyrosine hydroxylase. The mRNA transcripts and protein of MOR were expressed in the atrial posterior wall tissue. MOR immunoreactive products were mainly distributed in the cell bodies of ICG neurons, primarily in parasympathetic and sympathetic neurons.(2) Compared with the Normal group, the expression ofMORmRNA and protein in ICG of the AF rat decreased(P<0.05). Compared with the AF-NS group, the duration of AF was shortened in the AF-EM2 group and AF-DAMGO group, and the expression of CX43 increased(P<0.05). Conclusion MOR is mainly expressed in sympathetic and parasympathetic neurons in ICG. The expression of MOR decreases in AF rats. MOR agonists alleviate AF.

Objective : To explore the expression of the μ⁃opioid receptor ( MOR) and the effects of intracellular vesicle transport on the MOR expression during endomorphin 2 ( EM2) analgesia. Methods : Adult male SD rats were randomly divided into 3 groups : control (naive) group , neuropathic pain group and drug group. Spared nerve injury (SNI) induced neuropathic pain rats were employed as the pain model. The drug group rats were the SNI pain ones intrathecally injected with EM2. The methods of immunofluorescence single staining and Western blot were used to detect the expression of MOR total protein , phosphorylated protein and Rab7 protein. Immunofluorescence double staining was used to detect the expression of MOR/Rab7 and MOR/LAMP1 co⁃labeled immunoreactivity. Results : Compared with the control group , the expression of total MOR protein and phosphorylated protein in the dorsal root ganglion (DRG) of the SNI pain rats decreased (P < 0. 05) , and the expression of Rab7 significantly increased (P < 0. 05) . The expression of MOR/Rab7 co⁃labeled immunoreactivity in Rab7 and MOR immunoreactive ( Ⅳir) products and MOR/LAMP1 co⁃labeled immunoreactivity in MOR and LAMP1 ⁃ir products both increased (P < 0. 05) . Multiple intrathecal injection of EM2 significantly increased paw withdrawal threshold in the SNI neuropathic pain rats (P < 0. 01) , the expression of MOR protein and phosphorylated protein in DRG was increased (P < 0. 05) , while the expression of Rab7 decreased (P < 0. 05) . Compared with the control group , the expression of MOR/Rab7 positive products in Rab7 and MOR positive ones decreased , and the expression of MOR/LAMP1 positive products in LAMP1 and MOR positive markers decreased ( P < 0. 05 ) . Conclusion In the process of analgesia , EM2 inhibits the expression of Rab7 in the DRG of SNI neuropathic pain rats , reduces the transport of MOR to lysosomes , and promotes the re⁃sensitization of MOR.