PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23719800-0 2013 Role of the major glutamate transporter GLT1 in nucleus accumbens core versus shell in cue-induced cocaine-seeking behavior. Cocaine 99-106 solute carrier family 1 member 2 Rattus norvegicus 40-44 23985782-0 2014 Chronic administration of the methylxanthine propentofylline impairs reinstatement to cocaine by a GLT-1-dependent mechanism. Cocaine 86-93 solute carrier family 1 member 2 Rattus norvegicus 99-104 23985782-7 2014 PPF restored the cocaine-induced decrease in GLT-1 in the accumbens core; then, using an antisense strategy against glutamate transporter GLT-1, we found that restored transporter expression was necessary for PPF to inhibit cue-primed cocaine seeking. Cocaine 17-24 solute carrier family 1 member 2 Rattus norvegicus 45-50 24612076-0 2015 Glutamate transporter GLT-1 mediates N-acetylcysteine inhibition of cocaine reinstatement. Cocaine 68-75 solute carrier family 1 member 2 Rattus norvegicus 22-27 24612076-2 2015 Cocaine self-administration in rats reduces both cystine-glutamate exchange and glutamate transport via GLT-1 in the nucleus accumbens, and NAC treatment normalizes these two glial processes critical for maintaining glutamate homeostasis. Cocaine 0-7 solute carrier family 1 member 2 Rattus norvegicus 104-109 24612076-9 2015 In contrast, suppressing NAC-induced restoration of GLT-1 not only prevented NAC from inhibiting reinstatement, but augmented the capacity of cues to reinstate cocaine seeking. Cocaine 160-167 solute carrier family 1 member 2 Rattus norvegicus 52-57 24612076-11 2015 Restoring GLT-1, not cystine-glutamate exchange, is a key mechanism whereby daily NAC reduces cue-induced cocaine reinstatement. Cocaine 106-113 solute carrier family 1 member 2 Rattus norvegicus 10-15 23719800-2 2013 Decreased expression of glutamate type I transporter (GLT1), which is responsible for >90% of glutamate clearance, occurs in the core of rats withdrawn from cocaine self-administration, while treatment with ceftriaxone, a beta-lactam antibiotic previously shown to increase GLT1 expression and function in rodents, upregulates GLT1 and attenuates cue-induced cocaine reinstatement. Cocaine 160-167 solute carrier family 1 member 2 Rattus norvegicus 54-58 23719800-2 2013 Decreased expression of glutamate type I transporter (GLT1), which is responsible for >90% of glutamate clearance, occurs in the core of rats withdrawn from cocaine self-administration, while treatment with ceftriaxone, a beta-lactam antibiotic previously shown to increase GLT1 expression and function in rodents, upregulates GLT1 and attenuates cue-induced cocaine reinstatement. Cocaine 362-369 solute carrier family 1 member 2 Rattus norvegicus 54-58 22433294-0 2012 Differential effects of cocaine access and withdrawal on glutamate type 1 transporter expression in rat nucleus accumbens core and shell. Cocaine 24-31 solute carrier family 1 member 2 Rattus norvegicus 57-85 22433294-3 2012 Consistent with this view, glutamate type 1 transporter (GLT1), the transporter responsible for >90% of glutamate uptake, is downregulated in NAc after several days of withdrawal in rats previously trained to self-administer cocaine under limited access conditions (1-2 h/d). Cocaine 228-235 solute carrier family 1 member 2 Rattus norvegicus 27-55 22433294-3 2012 Consistent with this view, glutamate type 1 transporter (GLT1), the transporter responsible for >90% of glutamate uptake, is downregulated in NAc after several days of withdrawal in rats previously trained to self-administer cocaine under limited access conditions (1-2 h/d). Cocaine 228-235 solute carrier family 1 member 2 Rattus norvegicus 57-61 22433294-5 2012 Here, we determined the combined effects of manipulating cocaine access and withdrawal on GLT1 expression in NAc core and shell. Cocaine 57-64 solute carrier family 1 member 2 Rattus norvegicus 90-94 33063090-3 2021 Previous findings revealed that cocaine and ethanol exposure downregulated GLT-1 and xCT, and that beta-lactam antibiotics restored their expression. Cocaine 32-39 solute carrier family 1 member 2 Rattus norvegicus 75-80 21524862-1 2011 BACKGROUND: The beta-lactam antibiotic and glutamate transporter subtype 1 (GLT-1) activator ceftriaxone prevents relapse to cocaine-seeking and inhibits morphine-induced physical dependence and tolerance in rats, but its efficacy against amphetamine-induced behaviors is unknown. Cocaine 125-132 solute carrier family 1 member 2 Rattus norvegicus 43-81 19625514-0 2009 Upregulation of GLT1 attenuates cue-induced reinstatement of cocaine-seeking behavior in rats. Cocaine 61-68 solute carrier family 1 member 2 Rattus norvegicus 16-20 19625514-2 2009 Because GLT1 is responsible for the uptake of >or=90% of extracellular glutamate, we tested the hypothesis that increased GLT1 expression attenuates cocaine relapse. Cocaine 152-159 solute carrier family 1 member 2 Rattus norvegicus 125-129 19625514-8 2009 Our results suggest that glutamate plays a key role in cue-induced relapse to cocaine-seeking behavior, implicating GLT1 as a potential therapeutic target for cocaine addiction. Cocaine 78-85 solute carrier family 1 member 2 Rattus norvegicus 116-120 35065197-9 2022 We confirm that the CRS-induced facilitation of cocaine self-administration is associated with enduring GLT-1 downregulation, an increase of basal extracellular glutamate and postsynaptic structural plasticity in the NAcore. Cocaine 48-55 solute carrier family 1 member 2 Rattus norvegicus 104-109 35051699-1 2022 The beta-lactam antibiotic ceftriaxone (CTX) is a glutamate transporter subtype 1 (GLT-1) enhancer that reduces cocaine reinforcing efficacy and relapse in rats, but pharmacokinetic liabilities limit translational utility. Cocaine 112-119 solute carrier family 1 member 2 Rattus norvegicus 50-81 35051699-1 2022 The beta-lactam antibiotic ceftriaxone (CTX) is a glutamate transporter subtype 1 (GLT-1) enhancer that reduces cocaine reinforcing efficacy and relapse in rats, but pharmacokinetic liabilities limit translational utility. Cocaine 112-119 solute carrier family 1 member 2 Rattus norvegicus 83-88 35091501-6 2022 Selective downregulation of astrocytic GLT-1 expression in the NAc by GLT-1 antisense oligonucleotides also inhibited cocaine self-administration. Cocaine 118-125 solute carrier family 1 member 2 Rattus norvegicus 39-44 33986035-2 2021 In rodents, the glutamate transporter-1 (GLT-1) is downregulated in the nucleus accumbens following cocaine self-administration and increasing the expression and function of GLT-1 reduces the reinstatement of cocaine-seeking. Cocaine 100-107 solute carrier family 1 member 2 Rattus norvegicus 16-39 33986035-2 2021 In rodents, the glutamate transporter-1 (GLT-1) is downregulated in the nucleus accumbens following cocaine self-administration and increasing the expression and function of GLT-1 reduces the reinstatement of cocaine-seeking. Cocaine 100-107 solute carrier family 1 member 2 Rattus norvegicus 41-46 33986035-2 2021 In rodents, the glutamate transporter-1 (GLT-1) is downregulated in the nucleus accumbens following cocaine self-administration and increasing the expression and function of GLT-1 reduces the reinstatement of cocaine-seeking. Cocaine 209-216 solute carrier family 1 member 2 Rattus norvegicus 16-39 33986035-2 2021 In rodents, the glutamate transporter-1 (GLT-1) is downregulated in the nucleus accumbens following cocaine self-administration and increasing the expression and function of GLT-1 reduces the reinstatement of cocaine-seeking. Cocaine 209-216 solute carrier family 1 member 2 Rattus norvegicus 41-46 33986035-2 2021 In rodents, the glutamate transporter-1 (GLT-1) is downregulated in the nucleus accumbens following cocaine self-administration and increasing the expression and function of GLT-1 reduces the reinstatement of cocaine-seeking. Cocaine 209-216 solute carrier family 1 member 2 Rattus norvegicus 174-179 33063090-10 2021 GLT-1 and xCT expression were downregulated after cocaine and ethanol co-exposure in the NAc core and shell, but not in dmPFC. Cocaine 50-57 solute carrier family 1 member 2 Rattus norvegicus 0-5 30240589-10 2018 On the other hand, cocaine reduced SNAT 1/2 and GLT-1 levels in the NAc and PFC in CSDS females. Cocaine 19-26 solute carrier family 1 member 2 Rattus norvegicus 48-53 32099993-12 2020 RESULTS: Cocaine exposure induced an alcohol deprivation effect (ADE), which was associated in part by a decrease in the expression of GLT-1 and xCT in the nucleus accumbens (NAc) core. Cocaine 9-16 solute carrier family 1 member 2 Rattus norvegicus 135-140 31266052-8 2020 However, we noted significant changes in glutamate homeostasis in the NA core of cocaine + alcohol rats relative to rats consuming cocaine alone, such as increased surface GLT-1 expression and a lack of increase in glutamate efflux during reinstatement of cocaine-seeking. Cocaine 81-88 solute carrier family 1 member 2 Rattus norvegicus 172-177 30144237-6 2019 In response to ShA and LgA cocaine intake, SLC1A2 and Grin1 mRNA levels decreased in SERT+/+ rats to levels equal of those of SERT-/- rats. Cocaine 27-34 solute carrier family 1 member 2 Rattus norvegicus 43-49 30716289-2 2019 Cocaine, ethanol, and methamphetamine reduce the expression of cystine-glutamate antiporter (xCT) and primary glial glutamate transporter 1 (GLT1) leading to increased extrasynaptic glutamate. Cocaine 0-7 solute carrier family 1 member 2 Rattus norvegicus 141-145 30714803-1 2019 Research using the cocaine self-administration and reinstatement animal model of relapse finds that the beta-lactam antibiotic, ceftriaxone, attenuates cocaine-primed reinstatement of cocaine seeking and upregulates two proteins that regulate glutamate release and reuptake (xCT and GLT-1, respectively) in the nucleus accumbens core (NAc). Cocaine 19-26 solute carrier family 1 member 2 Rattus norvegicus 283-288 30714803-12 2019 Furthermore, the upregulation of both GLT-1 and xCT in the NAc may be needed to attenuate cocaine seeking. Cocaine 90-97 solute carrier family 1 member 2 Rattus norvegicus 38-43 33065231-5 2020 We found reduced GLT-1 transcript and mRNA level in the prefrontal cortex (PFCTX) and dorsal striatum (DSTR) in rats that had previously self-administered cocaine after 3 days of extinction training, which was associated with downregulation of PAX6 (transcript and mRNA) and NFKB2 (mRNA) level in the PFCTX and with upregulation of miR-543-3p and miR-342-3p in the DSTR. Cocaine 155-162 solute carrier family 1 member 2 Rattus norvegicus 17-22 33065231-7 2020 In conclusion, 3-day drug-free period modulates GLT-1 and xCT gene expression through genetic and epigenetic mechanisms, and such changes in expression seem to be potential molecular targets for developing a treatment for cocaine-seeking behavior. Cocaine 222-229 solute carrier family 1 member 2 Rattus norvegicus 48-53 31100299-13 2019 Future experiments may resolve the question concerning whether modulation exclusively of the GLT-1 expression in the HIP may attenuate cocaine-induced place preference or relapse. Cocaine 135-142 solute carrier family 1 member 2 Rattus norvegicus 93-98 29567092-3 2018 Ceftriaxone restores cocaine-induced deficits in both system xc- and GLT-1 expression and function in the nucleus accumbens core (NAc). Cocaine 21-28 solute carrier family 1 member 2 Rattus norvegicus 69-74 29567092-4 2018 We recently demonstrated that restoration of GLT-1 expression in the NAc is necessary for ceftriaxone to attenuate reinstatement of cocaine-seeking. Cocaine 132-139 solute carrier family 1 member 2 Rattus norvegicus 45-50 28442364-3 2017 Cocaine exposure has been shown to induce a dysregulation in glutamate homeostasis and a decrease in the expression of GLT-1 and xCT in the nucleus accumbens (NAc). Cocaine 0-7 solute carrier family 1 member 2 Rattus norvegicus 119-124 28990593-7 2018 Riluzole also reversed the cocaine-induced suppression of the high-affinity glutamate transporter 1 (EAAT2/GLT-1) in the nucleus accumbens (NAc). Cocaine 27-34 solute carrier family 1 member 2 Rattus norvegicus 101-106 28990593-7 2018 Riluzole also reversed the cocaine-induced suppression of the high-affinity glutamate transporter 1 (EAAT2/GLT-1) in the nucleus accumbens (NAc). Cocaine 27-34 solute carrier family 1 member 2 Rattus norvegicus 107-112 28990593-8 2018 GLT-1 is responsible for the majority of glutamate uptake in the brain, and has been previously reported to be downregulated by cocaine. Cocaine 128-135 solute carrier family 1 member 2 Rattus norvegicus 0-5 28919080-0 2018 Regulation of glutamate transporter 1 (GLT-1) gene expression by cocaine self-administration and withdrawal. Cocaine 65-72 solute carrier family 1 member 2 Rattus norvegicus 14-37 28919080-0 2018 Regulation of glutamate transporter 1 (GLT-1) gene expression by cocaine self-administration and withdrawal. Cocaine 65-72 solute carrier family 1 member 2 Rattus norvegicus 39-44 28919080-2 2018 The decrease in GLT-1 protein expression following cocaine self-administration is dependent on both the amount of cocaine self-administered and the length of withdrawal, with longer access to cocaine and longer withdrawal periods leading to greater decreases in GLT-1 protein. Cocaine 51-58 solute carrier family 1 member 2 Rattus norvegicus 16-21 28919080-2 2018 The decrease in GLT-1 protein expression following cocaine self-administration is dependent on both the amount of cocaine self-administered and the length of withdrawal, with longer access to cocaine and longer withdrawal periods leading to greater decreases in GLT-1 protein. Cocaine 114-121 solute carrier family 1 member 2 Rattus norvegicus 16-21 28919080-2 2018 The decrease in GLT-1 protein expression following cocaine self-administration is dependent on both the amount of cocaine self-administered and the length of withdrawal, with longer access to cocaine and longer withdrawal periods leading to greater decreases in GLT-1 protein. Cocaine 114-121 solute carrier family 1 member 2 Rattus norvegicus 16-21 28919080-3 2018 However, the mechanism(s) by which cocaine downregulates GLT-1 protein remains unknown. Cocaine 35-42 solute carrier family 1 member 2 Rattus norvegicus 57-62 28919080-5 2018 While downregulation of GLT-1 protein is observed following ShA cocaine self-administration and extinction, this model did not lead to a change in GLT-1A or GLT-1B gene expression in any brain region examined. Cocaine 64-71 solute carrier family 1 member 2 Rattus norvegicus 24-29 28919080-9 2018 In addition, LgA cocaine self-administration and withdrawal induced hypermethylation of the GLT-1 gene in the NAc. Cocaine 17-24 solute carrier family 1 member 2 Rattus norvegicus 92-97 28919080-10 2018 These results indicate that a decrease in NAc GLT-1 mRNA is only observed after extended access to cocaine combined with protracted abstinence, and that epigenetic mechanisms likely contribute to this effect. Cocaine 99-106 solute carrier family 1 member 2 Rattus norvegicus 46-51 28442364-11 2017 Co-exposure of cocaine and ethanol decreased the relative mRNA expression and the expression of GLT-1 in the NAc but not in the medial prefrontal cortex (mPFC). Cocaine 15-22 solute carrier family 1 member 2 Rattus norvegicus 96-101 28495973-12 2017 While upregulation of both xCT and GLT-1 are essential to the ability of ceftriaxone to attenuate cue-induced reinstatement of cocaine seeking, each protein uniquely affects the expression of other glutamate receptor and transporter proteins. Cocaine 127-134 solute carrier family 1 member 2 Rattus norvegicus 35-40 28495973-0 2017 Contrasting the Role of xCT and GLT-1 Upregulation in the Ability of Ceftriaxone to Attenuate the Cue-Induced Reinstatement of Cocaine Seeking and Normalize AMPA Receptor Subunit Expression. Cocaine 127-134 solute carrier family 1 member 2 Rattus norvegicus 32-37 27685834-7 2016 Previous studies have established a role for EAAT2-mediated re-uptake on reinstatement of cocaine seeking following extended withdrawal and extinction training. Cocaine 90-97 solute carrier family 1 member 2 Rattus norvegicus 45-50 27060486-11 2016 The present results along with previous reports of CEF"s efficacy in reducing cocaine self-administration in rats suggest that modulation of GLT-1 expression and/or activity is an important pharmacological target for treating polysubstance abuse and dependence. Cocaine 78-85 solute carrier family 1 member 2 Rattus norvegicus 141-146 27993695-3 2017 Parenteral treatment with ceftriaxone, beta-lactam antibiotic, has been reported to attenuate ethanol consumption and reinstatement to cocaine-seeking behavior, in part, by restoring the expression of GLT-1 and xCT in mesocorticolimbic brain regions in rats. Cocaine 135-142 solute carrier family 1 member 2 Rattus norvegicus 201-206