PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33559278-1 2021 Cocaine not only increases brain dopamine levels but also activates the sigma1 receptor (sigma1 R) that in turn regulates orexigenic receptor function. Cocaine 0-7 sigma non-opioid intracellular receptor 1 Mus musculus 72-87 33559278-8 2021 The functionality of the complex, able to couple to both Gs and Gq proteins, is affected by cocaine binding to the sigma1 R, as confirmed using samples from sigma1 R-/- mice. Cocaine 92-99 sigma non-opioid intracellular receptor 1 Mus musculus 115-123 33559278-8 2021 The functionality of the complex, able to couple to both Gs and Gq proteins, is affected by cocaine binding to the sigma1 R, as confirmed using samples from sigma1 R-/- mice. Cocaine 92-99 sigma non-opioid intracellular receptor 1 Mus musculus 157-165 33559278-1 2021 Cocaine not only increases brain dopamine levels but also activates the sigma1 receptor (sigma1 R) that in turn regulates orexigenic receptor function. Cocaine 0-7 sigma non-opioid intracellular receptor 1 Mus musculus 89-97 30151726-10 2019 Interventions aimed at blocking either the sigma-1 receptor or the upstream ER stress mediators could likely be envisioned as promising therapeutic targets for abrogating cocaine-mediated inflammation in pericytes. Cocaine 171-178 sigma non-opioid intracellular receptor 1 Mus musculus 43-59 32822804-10 2020 Our results suggest that GPx-1 is a critical mediator for the attenuation of cocaine-induced behavioral sensitization via modulating sigma-1 receptor-mediated ERK activation by the induction of the Nrf2-related system. Cocaine 77-84 sigma non-opioid intracellular receptor 1 Mus musculus 133-149 31139878-1 2019 RATIONALE: Previous research indicates that the selective sigma-1 receptor ligand PD144418 and the selective sigma-2 ligands YUN-252 can inhibit cocaine-induced hyperactivity. Cocaine 145-152 sigma non-opioid intracellular receptor 1 Mus musculus 58-74 31596232-5 2019 The release of EVs occurs when cocaine causes dissociation of the Sig-1R from ADP-ribosylation factor (ARF6), a G-protein regulating EV trafficking, leading to activation of myosin light chain kinase (MLCK). Cocaine 31-38 sigma non-opioid intracellular receptor 1 Mus musculus 66-72 31596232-6 2019 Blockade of Sig-1R function, or inhibition of ARF6 or MLCK also prevented cocaine-induced EV release and cocaine-stimulated 2-AG-modulation of inhibitory synapses in DA neurons. Cocaine 74-81 sigma non-opioid intracellular receptor 1 Mus musculus 12-18 31596232-6 2019 Blockade of Sig-1R function, or inhibition of ARF6 or MLCK also prevented cocaine-induced EV release and cocaine-stimulated 2-AG-modulation of inhibitory synapses in DA neurons. Cocaine 105-112 sigma non-opioid intracellular receptor 1 Mus musculus 12-18 31596232-7 2019 Our results implicate the Sig-1R-ARF6 complex in control of EV release and demonstrate that cocaine-mediated 2-AG release can occur via EVs. Cocaine 92-99 sigma non-opioid intracellular receptor 1 Mus musculus 26-32 31332816-0 2019 Glutathione peroxidase-1 gene rescues cocaine-induced conditioned place preference in mice by inhibiting sigma-1 receptor expression. Cocaine 38-45 sigma non-opioid intracellular receptor 1 Mus musculus 105-121 31332816-2 2019 Cocaine-induced CPP was accompanied by an increase in the level of sigma-1 receptor in the nucleus accumbens (NAc). Cocaine 0-7 sigma non-opioid intracellular receptor 1 Mus musculus 67-83 31332816-5 2019 Treatment of the mice with BD1047, a sigma-1 receptor antagonist, significantly attenuated both cocaine-induced CPP and c-Fos-immunoreactivity (c-Fos-IR) in WT and GPx-1 KO mice, although the effects were more evident in the latter group. Cocaine 96-103 sigma non-opioid intracellular receptor 1 Mus musculus 37-53 31332816-7 2019 Overall, our results suggest that GPx-1 attenuates cocaine-induced CPP via inhibition of sigma-1 receptor expression. Cocaine 51-58 sigma non-opioid intracellular receptor 1 Mus musculus 89-105 30639509-4 2019 sigma1 receptor antagonist PD144418 has been found to produce a dose-dependent attenuation of locomotor activity induced by cocaine, and by itself, does not suppress basal locomotor activity in mice. Cocaine 124-131 sigma non-opioid intracellular receptor 1 Mus musculus 0-15 24599455-6 2014 Using in vitro assays with transfected cells and in ex vivo experiments using both rats acutely treated or self-administered with cocaine along with mice depleted of sigma1 receptor, we show that blockade of sigma1 receptor by an antagonist restores the protective H3 receptor-mediated brake on D1 receptor signaling and prevents the cell death from elevated D1 receptor signaling. Cocaine 130-137 sigma non-opioid intracellular receptor 1 Mus musculus 208-223 24194528-9 2014 The sigma1-receptor antagonist BD 1008 [N-[2-(3,4-dichlorophenyl)ethyl]-N-methyl-2-(1-pyrrolidinyl)ethylamine dihydrobromide] blocked the locomotor-stimulant effects of cocaine. Cocaine 169-176 sigma non-opioid intracellular receptor 1 Mus musculus 4-19 23637801-4 2013 Exploring the effect of cocaine on dopamine D2 receptors function, we present evidence of sigma1 receptor molecular and functional interaction with dopamine D2 receptors. Cocaine 24-31 sigma non-opioid intracellular receptor 1 Mus musculus 90-105 20956312-4 2010 In the present study, D(1)R and sigma(1)R were found to heteromerize in transfected cells, where cocaine robustly potentiated D(1)R-mediated adenylyl cyclase activation, induced MAPK activation per se and counteracted MAPK activation induced by D(1)R stimulation in a dopamine transporter-independent and sigma(1)R-dependent manner. Cocaine 97-104 sigma non-opioid intracellular receptor 1 Mus musculus 32-41 20956312-4 2010 In the present study, D(1)R and sigma(1)R were found to heteromerize in transfected cells, where cocaine robustly potentiated D(1)R-mediated adenylyl cyclase activation, induced MAPK activation per se and counteracted MAPK activation induced by D(1)R stimulation in a dopamine transporter-independent and sigma(1)R-dependent manner. Cocaine 97-104 sigma non-opioid intracellular receptor 1 Mus musculus 305-314 20956312-6 2010 Therefore, these results provide a molecular explanation for which D(1)R plays a more significant role in the behavioral effects of cocaine, through sigma(1)R-D(1)R heteromerization, and provide a unique perspective toward understanding the molecular basis of cocaine addiction. Cocaine 132-139 sigma non-opioid intracellular receptor 1 Mus musculus 149-158 18591217-0 2008 Alterations in fos-related antigen 2 and sigma1 receptor gene and protein expression are associated with the development of cocaine-induced behavioral sensitization: time course and regional distribution studies. Cocaine 124-131 sigma non-opioid intracellular receptor 1 Mus musculus 41-56 18591217-2 2008 Earlier studies demonstrated that acute administration of cocaine up-regulates the immediate-early gene fos-related antigen 2 (fra-2) followed by a later up-regulation of sigma(1) receptor gene and protein levels in brain regions involved in addiction and reward. Cocaine 58-65 sigma non-opioid intracellular receptor 1 Mus musculus 171-188 18591217-4 2008 Using a cocaine-induced behavioral sensitization model coupled with gene and protein expression studies in mice, the results show that cocaine induces the expression of fra-2, which leads to a progressive increase in sigma(1) receptor gene and protein expression over a period of days. Cocaine 8-15 sigma non-opioid intracellular receptor 1 Mus musculus 217-234 18591217-4 2008 Using a cocaine-induced behavioral sensitization model coupled with gene and protein expression studies in mice, the results show that cocaine induces the expression of fra-2, which leads to a progressive increase in sigma(1) receptor gene and protein expression over a period of days. Cocaine 135-142 sigma non-opioid intracellular receptor 1 Mus musculus 217-234 18591217-6 2008 The cocaine-induced changes in fra-2 and sigma(1) receptor gene and protein expression occur in brain regions that subserve drug abuse, such as the cortex, striatum, and hippocampus, but not the cerebellum. Cocaine 4-11 sigma non-opioid intracellular receptor 1 Mus musculus 41-58 18591217-7 2008 Moreover, the prototypic sigma(1) receptor antagonist 1-[2-(3,4-dichloropheny)ethyl]-4-methylpiperazine (BD1063) significantly attenuates both the molecular adaptations and behavioral sensitization induced by cocaine. Cocaine 209-216 sigma non-opioid intracellular receptor 1 Mus musculus 25-42 18591217-8 2008 These data suggest that repeated exposure to cocaine elicits alterations in fra-2 and sigma(1) receptor-mediated mechanisms, which ultimately manifest as altered behavioral responses to cocaine. Cocaine 45-52 sigma non-opioid intracellular receptor 1 Mus musculus 86-103 18591217-8 2008 These data suggest that repeated exposure to cocaine elicits alterations in fra-2 and sigma(1) receptor-mediated mechanisms, which ultimately manifest as altered behavioral responses to cocaine. Cocaine 186-193 sigma non-opioid intracellular receptor 1 Mus musculus 86-103 16132061-0 2006 Sigma1 receptor ligands and related neuroactive steroids interfere with the cocaine-induced state of memory. Cocaine 76-83 sigma non-opioid intracellular receptor 1 Mus musculus 0-15 16132061-1 2006 The present series of experiments examined the involvement of the sigma(1) receptor and related neuroactive steroids in the memory state induced by a very low dose of cocaine. Cocaine 167-174 sigma non-opioid intracellular receptor 1 Mus musculus 66-83 16132061-6 2006 Since sigma(1) receptor activation is an important event during the acquisition of cocaine reward, we tested several sigma(1) ligands and related neurosteroids. Cocaine 83-90 sigma non-opioid intracellular receptor 1 Mus musculus 6-23 16132061-11 2006 This study demonstrated that: (i) low doses of cocaine induce a chemical state/memory trace sustaining StD; (ii) modulation of the sigma(1) receptor activation, although insufficient to provoke StD, modulates the cocaine state; (iii) neuroactive steroids exert a unique role in state-dependent vs state-independent learning, via GABA(A) or sigma(1) receptor modulation, and are able to affect the cocaine-induced mnesic trace at low brain concentrations. Cocaine 47-54 sigma non-opioid intracellular receptor 1 Mus musculus 131-148 16132061-11 2006 This study demonstrated that: (i) low doses of cocaine induce a chemical state/memory trace sustaining StD; (ii) modulation of the sigma(1) receptor activation, although insufficient to provoke StD, modulates the cocaine state; (iii) neuroactive steroids exert a unique role in state-dependent vs state-independent learning, via GABA(A) or sigma(1) receptor modulation, and are able to affect the cocaine-induced mnesic trace at low brain concentrations. Cocaine 47-54 sigma non-opioid intracellular receptor 1 Mus musculus 340-357 16132061-11 2006 This study demonstrated that: (i) low doses of cocaine induce a chemical state/memory trace sustaining StD; (ii) modulation of the sigma(1) receptor activation, although insufficient to provoke StD, modulates the cocaine state; (iii) neuroactive steroids exert a unique role in state-dependent vs state-independent learning, via GABA(A) or sigma(1) receptor modulation, and are able to affect the cocaine-induced mnesic trace at low brain concentrations. Cocaine 213-220 sigma non-opioid intracellular receptor 1 Mus musculus 131-148 16132061-11 2006 This study demonstrated that: (i) low doses of cocaine induce a chemical state/memory trace sustaining StD; (ii) modulation of the sigma(1) receptor activation, although insufficient to provoke StD, modulates the cocaine state; (iii) neuroactive steroids exert a unique role in state-dependent vs state-independent learning, via GABA(A) or sigma(1) receptor modulation, and are able to affect the cocaine-induced mnesic trace at low brain concentrations. Cocaine 213-220 sigma non-opioid intracellular receptor 1 Mus musculus 131-148 15879001-0 2005 Cocaine up-regulates Fra-2 and sigma-1 receptor gene and protein expression in brain regions involved in addiction and reward. Cocaine 0-7 sigma non-opioid intracellular receptor 1 Mus musculus 31-47 15879001-2 2005 A previous study revealed that the immediate early gene fra-2 is up-regulated after cocaine administration, and this effect is prevented by the sigma-1 receptor antagonist BD1063 [1-[2-(3,4-dichlorophenyl)ethyl]-4-methylpiperazine]. Cocaine 84-91 sigma non-opioid intracellular receptor 1 Mus musculus 144-160 15879001-7 2005 The cocaine-induced up-regulation of fra-2 and sigma-1 receptor genes and proteins were detected in whole brain, striatum, and cortex, but not in cerebellum. Cocaine 4-11 sigma non-opioid intracellular receptor 1 Mus musculus 47-63 15770241-6 2005 Our analyses demonstrate that repeated cocaine administration induces changes in the expression of 109 genes, including those encoding the stromal cell-derived factor I, insulin-like growth factor binding protein 6, sigma 1 receptor, regulators of G-protein signaling protein 4, Wnt1 responsive Cdc42 homolog, Ca2+/calmodulin-dependent protein kinase II alpha subunit, and cyclin D2, via the D1 receptors. Cocaine 39-46 sigma non-opioid intracellular receptor 1 Mus musculus 216-232 14741436-2 2004 Administration of cocaine to mice promoted the in vivo growth of a syngeneic lung cancer cell line and identical effects were observed with PRE 084, a selective sigma(1) receptor agonist. Cocaine 18-25 sigma non-opioid intracellular receptor 1 Mus musculus 161-178 15547786-0 2004 Involvement of the sigma1 receptor in the appetitive effects of cocaine. Cocaine 64-71 sigma non-opioid intracellular receptor 1 Mus musculus 19-34 15547786-4 2004 We will describe thereafter the recent results showing that activation of the sigma (1) receptor is also involved in the appetitive properties of cocaine, as measured using place preference conditioning in mice. Cocaine 146-153 sigma non-opioid intracellular receptor 1 Mus musculus 78-96 15547786-6 2004 The observation that repeated administration of cocaine rapidly provokes overexpression of the sigma (1) receptor outlines its major role in these first psychological steps of addictive processes. Cocaine 48-55 sigma non-opioid intracellular receptor 1 Mus musculus 95-113 14985920-0 2004 The sigma1 (sigma1) receptor activation is a key step for the reactivation of cocaine conditioned place preference by drug priming. Cocaine 78-85 sigma non-opioid intracellular receptor 1 Mus musculus 4-28 14985920-2 2004 Such approach allowed to previously demonstrate the importance of the neuromodulatory sigma1 (sigma1) receptor in acquisition of cocaine-induced CPP. Cocaine 129-136 sigma non-opioid intracellular receptor 1 Mus musculus 86-110 14985920-11 2004 Moreover, the in vivo [3H](+)-SKF-10,047 binding levels to the sigma1 receptor were increased after cocaine conditioning in numerous brain structures and these increases subsisted after extinction. Cocaine 100-107 sigma non-opioid intracellular receptor 1 Mus musculus 63-78 14741436-5 2004 We conclude that sigma(1) receptor ligands, including cocaine, augment tumor growth via a cytokine-dependent, receptor-mediated mechanism that involves regulation of T helper 1/T helper 2 cytokine balance. Cocaine 54-61 sigma non-opioid intracellular receptor 1 Mus musculus 17-34 12736327-12 2003 These results showed that neuroactive steroids play a role in cocaine-induced appetence, through their interaction with the sigma1 receptor. Cocaine 62-69 sigma non-opioid intracellular receptor 1 Mus musculus 124-139 12736327-0 2003 Sigma 1 receptor-related neuroactive steroids modulate cocaine-induced reward. Cocaine 55-62 sigma non-opioid intracellular receptor 1 Mus musculus 0-16 12736327-1 2003 The sigma1 receptor is critically involved in the rewarding effect of cocaine, as measured using the conditioned place preference (CPP) procedure in mice. Cocaine 70-77 sigma non-opioid intracellular receptor 1 Mus musculus 4-19 10817525-6 1999 The obtained results indicate that panamesine, a selective sigma ligand with a preference for sigma1 receptor subtype and potential antagonistic activity, decreased the effects of cocaine. Cocaine 180-187 sigma non-opioid intracellular receptor 1 Mus musculus 94-109 11927169-0 2002 Involvement of the sigma(1) receptor in cocaine-induced conditioned place preference: possible dependence on dopamine uptake blockade. Cocaine 40-47 sigma non-opioid intracellular receptor 1 Mus musculus 19-36 11006959-0 2000 Involvement of the sigma1 receptor in the cocaine-induced conditioned place preference. Cocaine 42-49 sigma non-opioid intracellular receptor 1 Mus musculus 19-34 11006959-1 2000 The sigma1 (sigma1) receptor constitutes a particular target of cocaine believed to be involved in some of its behavioral effects. Cocaine 64-71 sigma non-opioid intracellular receptor 1 Mus musculus 4-28 11006959-7 2000 The sigma1 receptor thus appears to be critically involved in the development of the cocaine-induced CPP and, in consequence, may constitute a promising approach to blocking cocaine reward. Cocaine 85-92 sigma non-opioid intracellular receptor 1 Mus musculus 4-19 11006959-7 2000 The sigma1 receptor thus appears to be critically involved in the development of the cocaine-induced CPP and, in consequence, may constitute a promising approach to blocking cocaine reward. Cocaine 174-181 sigma non-opioid intracellular receptor 1 Mus musculus 4-19 12028363-11 2002 Noteworthy, these observations are coherent with strain differences observed in the intensity of cocaine-induced reward properties, known to critically involve the sigma(1) receptor. Cocaine 97-104 sigma non-opioid intracellular receptor 1 Mus musculus 164-181 11927169-1 2002 The involvement of the sigma(1) receptor on the rewarding effects of cocaine was examined using the conditioned place preference (CPP) procedure in C57BL/6 mice. Cocaine 69-76 sigma non-opioid intracellular receptor 1 Mus musculus 23-40 11927169-5 2002 Moreover, the CPP induced by N-[1-(2-benzo(b)thiophenyl)cyclohexyl]piperidine (BTCP), a selective dopamine reuptake inhibitor, was blocked by treatments with the sigma(1) receptor antagonists as was similarly observed with cocaine. Cocaine 223-230 sigma non-opioid intracellular receptor 1 Mus musculus 162-179 11927169-6 2002 In addition, the repetitive treatment with cocaine during conditioning increased sigma(1) receptor mRNA expression in the nucleus accumbens, but not in the caudate putamen, prefrontal cortex or cerebellum. Cocaine 43-50 sigma non-opioid intracellular receptor 1 Mus musculus 81-98 11927169-7 2002 These data show that the sigma(1) receptor is not only necessary for acquisition of the cocaine-induced CPP, but that it is also implicated in its expression, confirming that activation of the sigma(1) receptor is induced during cocaine"s early effects. Cocaine 88-95 sigma non-opioid intracellular receptor 1 Mus musculus 25-42 11927169-7 2002 These data show that the sigma(1) receptor is not only necessary for acquisition of the cocaine-induced CPP, but that it is also implicated in its expression, confirming that activation of the sigma(1) receptor is induced during cocaine"s early effects. Cocaine 88-95 sigma non-opioid intracellular receptor 1 Mus musculus 193-210 11927169-10 2002 These results show that strategies targeting the sigma(1) receptor with selective antagonists may allow effective attenuation of cocaine"s rewarding properties and, in turn, offer new treatment strategies against drug addiction. Cocaine 129-136 sigma non-opioid intracellular receptor 1 Mus musculus 49-66 10817525-8 1999 These findings support the idea that sigma2 receptor subtype is involved in psychomotor stimulant effects of cocaine while sigma1 receptor subtype participates in the cocaine-induced convulsions. Cocaine 167-174 sigma non-opioid intracellular receptor 1 Mus musculus 123-138