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研究目的: Theanteriorcingulatecortex(ACC)playsakeyroleinregulatingmoodinanimals,especiallyanxiety,andisalsoabrainregionthatis indispensable to pain perception.Postoperative anxiety is closely related to the experience of pain.Remifentanil is a commonly used surgical analgesic.The mechanism of supraspinal hyperalgesia caused by remifentanil remains unclear.研究方法: We used animal models to simulate postoperative hyperalgesia and studied the GluR1 AMPA receptor subunit in the ACC using western blots and immunocytochemistry.Behavioral tests were used to estimate anxiety levels.We found no significant change in GluR1 levels before and after hyperalgesia,whereasphosphorylationofGluR1Ser845 wassignificantlyincreasedafterhyperalgesia.Doublestainingforc-Fos,widely used as a marker of neural activation,and Arc,which facilitates GluR1 endocytosis,revealed that neural activation increased and the expressionofArcdecreasedafterhyperalgesia.LocalinjectionofaproteinkinaseAinhibitor(H89)intheACCeffectivelyblockedthe phosphorylationofGluR1Ser845 andalleviatedthehyperalgesiaandanxietyshowninthebehavioraltests.Doublestainingreveal edno significant changein c-Fos 研究结果: Local injection of ibotenic acidcaused damage totheACC,followingwhichremifentanildidnotinducehyperalgesiaoranxiety.Theseresultsleadustoconc ludethattheACCisacriticalhubfor remifentanil-induced hyperalgesia(RIH)and RIHrelated anxiety and that regulating the phosphorylation of GluR1Ser845 may modulate RIH and anxiety.研究结论: Anxiety may be an influential factor contributing to individual differences in RIH occurrence.