PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29434817-0 2018 Delta-opioid receptor inhibition prevents remifentanil-induced post-operative hyperalgesia via regulating GluR1 trafficking and AMPA receptor function. Remifentanil 42-54 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 106-111 33779892-8 2021 Taken together, these findings suggest that TMEM16C/Slack regulation of excitatory synaptic plasticity via GluA1-containing AMPARs is critical in the pathogenesis of remifentanil-induced postoperative hyperalgesia in rats. Remifentanil 166-178 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 107-112 33779892-8 2021 Taken together, these findings suggest that TMEM16C/Slack regulation of excitatory synaptic plasticity via GluA1-containing AMPARs is critical in the pathogenesis of remifentanil-induced postoperative hyperalgesia in rats. Remifentanil 166-178 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 124-130 31430547-0 2019 Chemokine CCL7 regulates spinal phosphorylation of GluA1-containing AMPA receptor via interleukin-18 in remifentanil-induced hyperalgesia in rats. Remifentanil 104-116 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 51-56 31430547-8 2019 RESULTS: We reported that acute exposure to remifentanil caused and maintained behavioral RIH with up-regulation of expression in CCL7/CCR2 and IL-18/IL-18R and the phosphorylation of GluA1 in the dorsal horn. Remifentanil 44-56 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 184-189 31430547-12 2019 CONCLUSION: Our current findings demonstrate that spinal CCL7/CCR2 modulation of GluA1-containing AMPA receptor activation via IL-18 and IL-18R over-expression is an important pathogenesis of remifentanil-induced hyperalgesia in rats. Remifentanil 192-204 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 81-86 29434817-9 2018 Remifentanil infusion led to upregulation of membrane expression of the AMPAR subunit GluR1 and DOR (P=0.003 and 0.001, respectively) no change in total GluR1 and DOR expression levels (P=0.244 and 0.531, respectively). Remifentanil 0-12 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 86-91 29434817-13 2018 Combined behavioral, western blot and electrophysiological evidence indicated that remifentanil-induced hyperalgesia was mediated by DOR activation, followed by phosphorylation-dependent GluR1 trafficking and AMPAR function enhancement in the spinal cord. Remifentanil 83-95 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 187-192 29578864-10 2018 Protein kinase Mzeta inhibitor reduced remifentanil-induced hyperalgesia, Kalirin-7 expression, and GluA1 trafficking. Remifentanil 39-51 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 100-105 29578864-14 2018 CONCLUSIONS: Spinal protein kinase Mzeta regulation of GluA1-containing AMPA receptor trafficking and spine morphology via Kalirin-7 overexpression is a fundamental pathogenesis of remifentanil-induced hyperalgesia in rats. Remifentanil 181-193 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 55-60 29434817-2 2018 A previous study by our group suggested that the trafficking and function of glutamate receptor 1 (GluR1) subunits contributes to remifentanil-induced hyperalgesia by regulating the phosphorylation of GluR1 in dorsal horn neurons. Remifentanil 130-142 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 77-97 29434817-2 2018 A previous study by our group suggested that the trafficking and function of glutamate receptor 1 (GluR1) subunits contributes to remifentanil-induced hyperalgesia by regulating the phosphorylation of GluR1 in dorsal horn neurons. Remifentanil 130-142 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 99-104 29434817-2 2018 A previous study by our group suggested that the trafficking and function of glutamate receptor 1 (GluR1) subunits contributes to remifentanil-induced hyperalgesia by regulating the phosphorylation of GluR1 in dorsal horn neurons. Remifentanil 130-142 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 201-206 27537764-11 2016 Besides, remifentanil infusion increased the expression of PICK1 mRNA and protein (P < .0001) and the membrane GluR1 and GluR2 internalization in spinal dorsal horn neurons (P < .0011). Remifentanil 9-21 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 114-119 25126703-7 2014 RESULTS: Membrane AMPAR subunit GluR1 was upregulated in the spinal cord in remifentanil-induced postoperative hyperalgesia rats (275 +- 36.54 [mean +- SD] vs 100 +- 9.53, P = 0.0009). Remifentanil 76-88 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 32-37 25126703-8 2014 Selective GSK-3beta inhibitors, LiCl and TDZD, treatment ameliorates remifentanil-induced postoperative hyperalgesia, and this was associated with the downregulated GluR1 subunit in the membrane fraction (254 +- 23.51 vs 119 +- 14.74, P = 0.0027; 254 +- 23.51 vs 124 +- 9.35, P = 0.0032). Remifentanil 69-81 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 165-170 25126703-11 2014 CONCLUSIONS: These results indicate that amelioration of remifentanil-induced postoperative hyperalgesia by GSK-3beta inhibition is attributed to downregulated AMPAR GluR1 expression in the membrane fraction and inhibition of AMPAR function via altering pGluR1 and Rab5 expression in the spinal dorsal horn. Remifentanil 57-69 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 166-171