PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16037950-0 2005 Increased AMPA GluR1 receptor subunit labeling on the plasma membrane of dendrites in the basolateral amygdala of rats self-administering morphine. Morphine 138-146 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 15-20 18294632-0 2008 Chronic administration of morphine is associated with a decrease in surface AMPA GluR1 receptor subunit in dopamine D1 receptor expressing neurons in the shell and non-D1 receptor expressing neurons in the core of the rat nucleus accumbens. Morphine 26-34 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 81-86 18294632-3 2008 Immunogold electron microscopy was used to quantify the surface expression of the AMPA GluR1 subunit in dendritic profiles of neurons in the Acb in response to intermittent 14-day non-contingent injections of escalating doses of morphine, a model that parallels opioid self-administration. Morphine 229-237 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 87-92 18294632-6 2008 We provide the first report that chronic morphine administration is associated with a receptor-phenotypic decrease in surface trafficking of GluR1 in Acb subregions. Morphine 41-49 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 141-146 18294632-7 2008 When compared to saline injected animals, morphine produced a decrease in plasma membrane GluR1 labeling in medium- and large-sized D1R expressing dendritic profiles in the Acb shell. Morphine 42-50 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 90-95 18294632-9 2008 These results indicate that chronic intermittent injection of escalating doses of morphine is accompanied by ultrastructural plasticity of GluR1 in neurons that are responsive to glutamate and dopamine-induced D1R activation in the Acb shell, and neurons capable of responding to glutamate but not D1R receptor stimulation in the Acb core. Morphine 82-90 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 139-144 16687214-3 2006 We found that repeated administration of morphine significantly elevated aAbs levels to MDOR and to the AMPA GluR1 subunit, but not to the NMDA NR2 subunit. Morphine 41-49 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 109-114 16775132-4 2006 However, the roles of D1 receptors, CREB, and GluR1 in morphine dependence are not well understood. Morphine 55-63 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 46-51 16775132-7 2006 Surprisingly, SKF 82958 increased P-GluR1, but not P-CREB, in the NAc, and naloxone reduced SKF 82958-mediated P-GluR1 induction specifically in morphine-dependent rats. Morphine 145-153 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 113-118 16775132-10 2006 These data raise the possibility that the rewarding effects of SKF 82958 in morphine-dependent rats involve increased P-GluR1 in the NAc, although the involvement of other brain regions cannot be ruled out. Morphine 76-84 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 120-125 16037950-4 2005 High-resolution immunogold electron microscopic immunocytochemistry was used to compare surface and intracellular labeling of the calcium sensitive AMPA GluR1 receptor subunit in the basolateral (BLA) and central (CeA) nuclei of the amygdala in rats self-administering escalating doses of morphine or saline. Morphine 289-297 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 153-158 16037950-5 2005 Morphine self-administration was associated with regionally diverse effects on dendritic GluR1 targeting in the BLA and CeA. Morphine 0-8 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 89-94 16037950-6 2005 In the BLA of morphine self-administering animals, there was a significant increase in the proportion of immunogold particles for GluR1 on the plasma membrane of dendrites, particularly in association with extrasynaptic sites, which was most prominent in large (2-4 microm) profiles. Morphine 14-22 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 130-135 16037950-9 2005 These results indicate that GluR1 targeting is a dynamic process that can be differentially affected in distinct amygdala regions in response to chronic self-administration of morphine. Morphine 176-184 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 28-33 15183518-6 2004 Caspace 1, D2 dopamine receptor, GABA-A alpha1 subunit, GRIA 1/3/4, Galphai2, PSD-95 and CREB were down-regulated in the NAc shell with morphine administration. Morphine 136-144 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 33-66 15287884-8 2004 The phosphorylation levels of GluR1 and NR1 subunits decreased in parallel with those of phospho-Thr-34 DARPP-32, supporting the hypothesis that morphine challenge elicited a decrease in PKA activity in morphine-sensitized rats. Morphine 145-153 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 30-35 15183518-9 2004 Specifically, GABA-A alpha1 subunit, GRIA1 subunit and PSD-95 mRNAs were decreased in the shell but increased in the core following morphine administration. Morphine 132-140 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 37-42 10822164-0 2000 An autoradiographic study of [3H]AMPA receptor binding and in situ hybridization of AMPA sensitive glutamate receptor A (GluR-A) subunits following morphine withdrawal in the rat brain. Morphine 148-156 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 99-119 10822164-0 2000 An autoradiographic study of [3H]AMPA receptor binding and in situ hybridization of AMPA sensitive glutamate receptor A (GluR-A) subunits following morphine withdrawal in the rat brain. Morphine 148-156 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 121-127 10684909-1 2000 Repeated administration of morphine increases expression of GluR1 (an AMPA glutamate receptor subunit) in the ventral tegmental area (VTA) of the midbrain, an important neural substrate for the rewarding actions of morphine. Morphine 27-35 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 60-65 10684909-1 2000 Repeated administration of morphine increases expression of GluR1 (an AMPA glutamate receptor subunit) in the ventral tegmental area (VTA) of the midbrain, an important neural substrate for the rewarding actions of morphine. Morphine 215-223 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 60-65 10684909-2 2000 Microinjections of a herpes simplex virus (HSV) vector that causes local overexpression of GluR1 (HSV-GluR1) into the VTA can enhance the ability of morphine to establish conditioned place preferences, suggesting that altered GluR1 expression in this region is directly associated with changes in the rewarding efficacy of morphine. Morphine 149-157 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 91-96 10684909-2 2000 Microinjections of a herpes simplex virus (HSV) vector that causes local overexpression of GluR1 (HSV-GluR1) into the VTA can enhance the ability of morphine to establish conditioned place preferences, suggesting that altered GluR1 expression in this region is directly associated with changes in the rewarding efficacy of morphine. Morphine 149-157 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 98-107 10684909-2 2000 Microinjections of a herpes simplex virus (HSV) vector that causes local overexpression of GluR1 (HSV-GluR1) into the VTA can enhance the ability of morphine to establish conditioned place preferences, suggesting that altered GluR1 expression in this region is directly associated with changes in the rewarding efficacy of morphine. Morphine 149-157 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 102-107 10684909-2 2000 Microinjections of a herpes simplex virus (HSV) vector that causes local overexpression of GluR1 (HSV-GluR1) into the VTA can enhance the ability of morphine to establish conditioned place preferences, suggesting that altered GluR1 expression in this region is directly associated with changes in the rewarding efficacy of morphine. Morphine 323-331 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 91-96 10684909-2 2000 Microinjections of a herpes simplex virus (HSV) vector that causes local overexpression of GluR1 (HSV-GluR1) into the VTA can enhance the ability of morphine to establish conditioned place preferences, suggesting that altered GluR1 expression in this region is directly associated with changes in the rewarding efficacy of morphine. Morphine 323-331 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 98-107 10684909-3 2000 We now report that in rats given HSV-GluR1 directly into the VTA, morphine is most rewarding when maximal transgene expression is in the rostral VTA, whereas morphine is aversive when maximal transgene expression is in the caudal VTA. Morphine 66-74 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 37-42 10684909-3 2000 We now report that in rats given HSV-GluR1 directly into the VTA, morphine is most rewarding when maximal transgene expression is in the rostral VTA, whereas morphine is aversive when maximal transgene expression is in the caudal VTA. Morphine 158-166 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 37-42 8613793-7 1996 Although morphine delivered by subcutaneous pellet implantation had no significant effect on subunit levels, morphine delivered intermittently by subcutaneous injections of escalating doses elevated GluR1 levels in the VTA. Morphine 109-117 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 199-204 27225765-5 2016 Here, we show that microinjection of the AMPAR antagonist NBQX into the NAc shell of morphine-dependent rats prevented naloxone-induced conditioned place aversions and decreases in sensitivity to brain stimulation reward, but had no effect on somatic withdrawal signs. Morphine 85-93 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 41-46 34390773-6 2021 In the NAc, morphine increased D1R, D2R, D3R, DAT, GluA1 and MOR immunoreactivity. Morphine 12-20 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 51-56 31863796-6 2020 Microinjection of NASPM, a selective inhibitor of homomeric GluA1-AMPARs, into CeA inhibited morphine intake. Morphine 93-101 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 60-65 31863796-7 2020 Furthermore, viral overexpression of GluA1 protein in CeA maintained morphine intake at a higher level than controls and reversed the pain-induced reduction in morphine intake. Morphine 69-77 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 37-42 31863796-7 2020 Furthermore, viral overexpression of GluA1 protein in CeA maintained morphine intake at a higher level than controls and reversed the pain-induced reduction in morphine intake. Morphine 160-168 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 37-42 31209728-6 2019 Results showed that membrane expression of GluA1 and GluA2 in the vmPFC was decreased following the recent retrieval, while the membrane expression of GluA1 and GluA2 in the vmPFC was increased following the remote retrieval of morphine-associated memory. Morphine 228-236 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 43-48 31209728-6 2019 Results showed that membrane expression of GluA1 and GluA2 in the vmPFC was decreased following the recent retrieval, while the membrane expression of GluA1 and GluA2 in the vmPFC was increased following the remote retrieval of morphine-associated memory. Morphine 228-236 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 151-156 27225765-8 2016 Naloxone decreased the surface/intracellular ratio and synaptosomal membrane levels of NAc GluA1 in morphine-dependent rats, suggesting a compensatory removal of AMPARs from synaptic zones. Morphine 100-108 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 91-96 27225765-9 2016 Together, these findings indicate that chronic morphine increases synaptic availability of GluA1-containing AMPARs in the NAc, which is necessary for triggering negative-affective states in response to naloxone. Morphine 47-55 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 91-96 27225765-9 2016 Together, these findings indicate that chronic morphine increases synaptic availability of GluA1-containing AMPARs in the NAc, which is necessary for triggering negative-affective states in response to naloxone. Morphine 47-55 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 108-114 27225765-13 2016 We use a rat model of morphine dependence to show that GluA1 subunits of AMPA glutamate receptors in the nucleus accumbens (NAc), a brain region critical for modulating affective states, are necessary for aversive effects of morphine withdrawal. Morphine 22-30 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 55-60 27225765-13 2016 We use a rat model of morphine dependence to show that GluA1 subunits of AMPA glutamate receptors in the nucleus accumbens (NAc), a brain region critical for modulating affective states, are necessary for aversive effects of morphine withdrawal. Morphine 225-233 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 55-60 27225765-14 2016 Using biochemical methods in NAc tissue, we show that morphine dependence increases cell surface expression of GluA1, suggesting that neurons in this area are primed for increased AMPA receptor activation upon withdrawal. Morphine 54-62 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 111-116 27225765-6 2016 Using a protein cross-linking approach, we found that the surface/intracellular ratio of NAc GluA1, but not GluA2, increased with morphine treatment, suggesting postsynaptic insertion of GluA2-lacking AMPARs. Morphine 130-138 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 93-98 27225765-6 2016 Using a protein cross-linking approach, we found that the surface/intracellular ratio of NAc GluA1, but not GluA2, increased with morphine treatment, suggesting postsynaptic insertion of GluA2-lacking AMPARs. Morphine 130-138 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 201-207 24201449-0 2014 Region-specific alterations in glutamate receptor 1 phosphorylation during context-induced drug seeking after withdrawal from morphine self-administration. Morphine 126-134 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 31-51 25746394-9 2015 CONCLUSIONS: Arc/Arg3.1 in the NAc shell mediates the reconsolidation of morphine-associated context memory via up-regulating the level of membrane of GluR1, for which the local activation of the ERK-CREB signal pathway, as an upstream mechanism of Arc/Arg3.1, is required. Morphine 73-81 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 151-156 25716866-4 2015 In the central nucleus of amygdala (CeA), a limbic structure critically involved in the affective dimension of pain, proteins of GluA1 subunits of glutamate AMPA receptors were upregulated during morphine withdrawal, and viral knockdown of CeA GluA1 eliminated the morphine-seeking behavior in withdrawn rats of the pain group. Morphine 196-204 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 129-134 25716866-4 2015 In the central nucleus of amygdala (CeA), a limbic structure critically involved in the affective dimension of pain, proteins of GluA1 subunits of glutamate AMPA receptors were upregulated during morphine withdrawal, and viral knockdown of CeA GluA1 eliminated the morphine-seeking behavior in withdrawn rats of the pain group. Morphine 265-273 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 129-134 25716866-7 2015 These results suggest direct MeCp2 repression of GluA1 function as a likely mechanism for morphine-seeking behavior maintained by long-lasting affective pain after morphine withdrawal. Morphine 90-98 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 49-54 25716866-7 2015 These results suggest direct MeCp2 repression of GluA1 function as a likely mechanism for morphine-seeking behavior maintained by long-lasting affective pain after morphine withdrawal. Morphine 164-172 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 49-54 25746394-0 2015 NAc Shell Arc/Arg3.1 Protein Mediates Reconsolidation of Morphine CPP by Increased GluR1 Cell Surface Expression: Activation of ERK-Coupled CREB is Required. Morphine 57-65 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 83-88 24201449-7 2014 These results suggest that time-dependent and region-specific changes in phosphorylation of GluR1 at Ser845, but not Ser831, are involved in the drug-seeking behavior elicited by re-exposure to the morphine-associated context. Morphine 198-206 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 92-97 23711322-5 2013 Acute morphine decreased GluA1 and GluA2 surface expression in mPFC and GluA1 in NAc. Morphine 6-14 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 25-30 23711322-5 2013 Acute morphine decreased GluA1 and GluA2 surface expression in mPFC and GluA1 in NAc. Morphine 6-14 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 72-77 23345231-3 2013 In CeA neurons, we found that CeA GluA1 expression was significantly increased 2 h after conditioning treatment with morphine, but not 24 h after the conditioning when the behavior of conditioned place reference (CPP) was fully established in rats. Morphine 117-125 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 34-39 23345231-4 2013 Adenoviral overexpression of GluA1 subunits in CeA accelerated associative learning, as shown by reduced minimum time of morphine conditioning required for CPP acquisition and by facilitated CPP extinction through extinction training with no morphine involved. Morphine 121-129 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 29-34 21175880-5 2011 Repeated morphine treatment decreased surface expression of GluA1 in the medial prefrontal cortex without affecting levels of GluA2. Morphine 9-17 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 60-65 19077125-0 2009 Extinction of morphine-dependent conditioned behavior is associated with increased phosphorylation of the GluR1 subunit of AMPA receptors at hippocampal synapses. Morphine 14-22 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 106-111 19077125-6 2009 Results showed that morphine-dependent CRs did not alter expression or redistribution of GluR1 or GluR2; however, the unpaired administration of morphine resulted in an increase in the phosphorylation of the GluR1 subunit at extrasynaptic sites. Morphine 145-153 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 208-213 18815253-0 2008 Region-specific changes in the subcellular distribution of AMPA receptor GluR1 subunit in the rat ventral tegmental area after acute or chronic morphine administration. Morphine 144-152 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 73-78 18815253-3 2008 Indeed, chronic morphine administration is known to increase AMPA receptor glutamate receptor 1 (GluR1) subunit in the VTA. Morphine 16-24 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 75-95 18815253-3 2008 Indeed, chronic morphine administration is known to increase AMPA receptor glutamate receptor 1 (GluR1) subunit in the VTA. Morphine 16-24 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 97-102 18815253-6 2008 Acute morphine administration produced a significant increase in GluR1 immunogold particles at the plasma membrane and postsynaptic densities in both TH- and non-TH-containing dendrites in the parabrachial VTA, a region that contains mainly prefrontal-cortical-projecting dopaminergic neurons involved in motivation and drug-seeking behavior. Morphine 6-14 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 65-70 18815253-7 2008 Chronic morphine administration maintained the increased synaptic GluR1 labeling in the parabrachial VTA, but also increased the number of GluR1-labeled synapses and TH immunoreactivity in dendrites of the paranigral VTA where substantially more dopaminergic neurons project to limbic structures implicated in locomotor activation and reward. Morphine 8-16 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 66-71 18815253-7 2008 Chronic morphine administration maintained the increased synaptic GluR1 labeling in the parabrachial VTA, but also increased the number of GluR1-labeled synapses and TH immunoreactivity in dendrites of the paranigral VTA where substantially more dopaminergic neurons project to limbic structures implicated in locomotor activation and reward. Morphine 8-16 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 139-144 18815253-8 2008 These results demonstrate a region- and dose-dependent redistribution of GluR1-containing AMPA receptors, which is consistent with acute morphine activation of cortical-projecting VTA neurons and chronic morphine activation of limbic-projecting VTA neurons. Morphine 137-145 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 73-78 18815253-8 2008 These results demonstrate a region- and dose-dependent redistribution of GluR1-containing AMPA receptors, which is consistent with acute morphine activation of cortical-projecting VTA neurons and chronic morphine activation of limbic-projecting VTA neurons. Morphine 204-212 glutamate ionotropic receptor AMPA type subunit 1 Rattus norvegicus 73-78