PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34445137-4 2021 This study investigated the consequences of ceftriaxone (CTX), an enhancer of glutamate transporter 1 expression, treatment on long-term synaptic potentiation (LTP) in the hippocampus of young rats. Ceftriaxone 44-55 solute carrier family 1 member 2 Rattus norvegicus 78-101 34409650-12 2021 Treatment with VPA or CEF enhanced the expression levels of GLT-1, GLAST, EAAC1, and GS, whereas the glutaminase expression level was reduced. Ceftriaxone 22-25 solute carrier family 1 member 2 Rattus norvegicus 60-65 34521349-11 2021 RESULTS: Compared with the TBI + vehicle group, the TBI + ceftriaxone 250 mg/kg group showed significantly lower ICP, improved motor dysfunction, reduced body weight loss, decreased infarct volume and neuronal apoptosis, decreased TBI-induced microglial activation and TNF-alpha expression in microglia, and increased GLT-1 expression in neurons and microglia. Ceftriaxone 58-69 solute carrier family 1 member 2 Rattus norvegicus 318-323 34521349-13 2021 CONCLUSIONS: The intraperitoneal injection of ceftriaxone with 250 mg/kg/day for three days may attenuate TBI by increasing GLT-1 expression and reducing neuroinflammation and neuronal apoptosis, thereby resulting in an improvement in functional outcomes, and this neuroprotective effect is not related to its antibacterial effects. Ceftriaxone 46-57 solute carrier family 1 member 2 Rattus norvegicus 124-129 34363739-10 2021 Our results showed that hippocampal microinjection of ceftriaxone, as an activator of GLT-1, reduced some signs of morphine withdrawal, such as activity, diarrhea, head tremor, freezing, and ptosis. Ceftriaxone 54-65 solute carrier family 1 member 2 Rattus norvegicus 86-91 33559250-10 2021 Ceftriaxone, a selective activator of GLT-1, obviously increased the PWT of CFA rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 38-43 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. Ceftriaxone 27-38 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. Ceftriaxone 27-38 solute carrier family 1 member 2 Rattus norvegicus 83-88 33986035-3 2021 The beta-lactam antibiotic ceftriaxone upregulates GLT-1 and attenuates cue- and cocaine-induced cocaine seeking without affecting motivation for natural rewards. Ceftriaxone 27-38 solute carrier family 1 member 2 Rattus norvegicus 51-56 33986035-5 2021 Thus, we aimed to develop novel molecules that retained the GLT-1 enhancing effects of ceftriaxone but displayed superior drug-like properties. Ceftriaxone 87-98 solute carrier family 1 member 2 Rattus norvegicus 60-65 34719508-9 2022 Furthermore, the GLT-1 agonist ceftriaxone showed a protective effect on TH-positive neuron impairment. Ceftriaxone 31-42 solute carrier family 1 member 2 Rattus norvegicus 17-22 33836247-0 2021 Ceftriaxone reduces waterpipe tobacco smoke withdrawal-induced anxiety in rats via modulating the expression of TNF-alpha/NFkB, Nrf2, and GLT-1. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 138-143 33075417-10 2020 Alternatively, treatment with ceftriaxone (CEF), a known GLT-1 upregulator, abolished the effect of chronic ethanol exposure on BDNF expression in the AcbSh. Ceftriaxone 30-41 solute carrier family 1 member 2 Rattus norvegicus 57-62 33075417-10 2020 Alternatively, treatment with ceftriaxone (CEF), a known GLT-1 upregulator, abolished the effect of chronic ethanol exposure on BDNF expression in the AcbSh. Ceftriaxone 43-46 solute carrier family 1 member 2 Rattus norvegicus 57-62 32382781-2 2020 While the restoration of nucleus accumbens core (NA core) GLT-1 expression is necessary for ceftriaxone to attenuate reinstatement, AAV-mediated GLT-1 overexpression is not sufficient to attenuate reinstatement and does not prevent glutamate efflux during reinstatement. Ceftriaxone 92-103 solute carrier family 1 member 2 Rattus norvegicus 58-63 32666660-1 2020 beta-Lactam antibiotics such as ceftriaxone, are potent stimulators of the expression of l-glutamate transporter GLT-1 and may exert neuroprotective effects when chronically used in rats and mice. Ceftriaxone 32-43 solute carrier family 1 member 2 Rattus norvegicus 113-118 32714151-0 2020 Ceftriaxone Relieves Trigeminal Neuropathic Pain Through Suppression of Spatiotemporal Synaptic Plasticity via Restoration of Glutamate Transporter 1 in the Medullary Dorsal Horn. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 126-149 32714151-4 2020 Western blot and immunofluorescent results demonstrated that 5-days administration of Cef resulted in the restoration of GLT-1 expression to a level equivalent to the sham control which was dramatically lost under the TNP condition. Ceftriaxone 86-89 solute carrier family 1 member 2 Rattus norvegicus 121-126 32714151-7 2020 Taken together, the results indicate that Cef can relieve TNP through suppression of spatiotemporal synaptic plasticity via GLT-1 restoration in the medullary dorsal horn of the trigeminal nerve. Ceftriaxone 42-45 solute carrier family 1 member 2 Rattus norvegicus 124-129 28257918-0 2017 Ceftriaxone-mediated upregulation of the glutamate transporter GLT-1 contrasts neurotoxicity evoked by kainate in rat organotypic spinal cord cultures. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 63-68 32008166-5 2020 Ceftriaxone is a beta-lactam antibiotic that upregulates GLT1 expression. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 57-61 32008166-6 2020 Bilateral microinjection of ceftriaxone recovered GLT1 expression, decreased synaptic C1q production, suppressed microglial phagocytosis of glutamatergic synapses in the hippocampal CA1, and attenuated synaptic and cognitive deficits in rats microinjected with Abeta1-40. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 50-54 31766528-0 2019 Ceftriaxone Treatment Affects EAAT2 Expression and Glutamatergic Neurotransmission and Exerts a Weak Anticonvulsant Effect in Young Rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 30-35 31766528-5 2019 Previous research showed that the antibiotic ceftriaxone (CTX) increased the expression and functional activity of excitatory amino acid transporter 2 (EAAT2) and exerted considerable anticonvulsant effects. Ceftriaxone 45-56 solute carrier family 1 member 2 Rattus norvegicus 115-150 31766528-5 2019 Previous research showed that the antibiotic ceftriaxone (CTX) increased the expression and functional activity of excitatory amino acid transporter 2 (EAAT2) and exerted considerable anticonvulsant effects. Ceftriaxone 45-56 solute carrier family 1 member 2 Rattus norvegicus 152-157 30716289-3 2019 Ceftriaxone (CTX) restores xCT and GLT1 expression and effectively suppresses cocaine and ethanol reinstatement, however, the effects of CTX on amphetamine (AMP) reinstatement are not determined. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 35-39 31178684-2 2019 Ceftriaxone (CEF) reduces excitotoxicity by increasing glutamate transporter 1 expression and glutamate reuptake. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 55-78 31178684-2 2019 Ceftriaxone (CEF) reduces excitotoxicity by increasing glutamate transporter 1 expression and glutamate reuptake. Ceftriaxone 13-16 solute carrier family 1 member 2 Rattus norvegicus 55-78 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). Ceftriaxone 128-139 solute carrier family 1 member 2 Rattus norvegicus 283-288 29567092-3 2018 Ceftriaxone restores cocaine-induced deficits in both system xc- and GLT-1 expression and function in the nucleus accumbens core (NAc). Ceftriaxone 0-11 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. Ceftriaxone 90-101 solute carrier family 1 member 2 Rattus norvegicus 45-50 29197981-2 2018 In male rats, ceftriaxone attenuates the reinstatement of cocaine-seeking while increasing glutamate transporter-1 (GLT-1) and xCT expression in the nucleus accumbens core (NAc). Ceftriaxone 14-25 solute carrier family 1 member 2 Rattus norvegicus 91-114 29197981-2 2018 In male rats, ceftriaxone attenuates the reinstatement of cocaine-seeking while increasing glutamate transporter-1 (GLT-1) and xCT expression in the nucleus accumbens core (NAc). Ceftriaxone 14-25 solute carrier family 1 member 2 Rattus norvegicus 116-121 29128307-7 2018 This reduction was restored by systemic administration of ceftriaxone, a beta-lactam antibiotic known to increase GLT-1 expression. Ceftriaxone 58-69 solute carrier family 1 member 2 Rattus norvegicus 114-119 29128307-9 2018 Finally, systemic administration of ceftriaxone alleviated depression- and anxiety-like behaviors, which was fully blocked by intra-LHb administrations of DHK, suggesting that GLT-1"s function in the LHb is critical. Ceftriaxone 36-47 solute carrier family 1 member 2 Rattus norvegicus 176-181 29045497-13 2017 Moreover, our results suggest that CEF and NAC may induce brain tolerance to ischemia by influencing GLT-1 and system xc- expression levels. Ceftriaxone 35-38 solute carrier family 1 member 2 Rattus norvegicus 101-106 28826758-1 2017 Studies from our laboratory showed that upregulation of glutamate transporter 1 (GLT-1) and cystine-glutamate exchanger (xCT) expression with ceftriaxone, beta-lactam antibiotic, in the brain was associated with attenuation of ethanol consumption. Ceftriaxone 142-153 solute carrier family 1 member 2 Rattus norvegicus 56-79 28826758-1 2017 Studies from our laboratory showed that upregulation of glutamate transporter 1 (GLT-1) and cystine-glutamate exchanger (xCT) expression with ceftriaxone, beta-lactam antibiotic, in the brain was associated with attenuation of ethanol consumption. Ceftriaxone 142-153 solute carrier family 1 member 2 Rattus norvegicus 81-86 28495973-4 2017 Intra-NAc xCT knockdown prevented ceftriaxone from attenuating reinstatement and from upregulating GLT-1 and resulted in increased surface expression of AMPA receptor subunits GluA1 and GluA2. Ceftriaxone 34-45 solute carrier family 1 member 2 Rattus norvegicus 99-104 28495973-5 2017 Intra-NAc GLT-1 knockdown also prevented ceftriaxone from attenuating reinstatement and from upregulating xCT expression, without affecting GluA1 and GluA2 expression. Ceftriaxone 41-52 solute carrier family 1 member 2 Rattus norvegicus 10-15 28495973-8 2017 These data support important and distinct roles for xCT and GLT-1 in the actions of ceftriaxone and add to a body of literature finding evidence for coregulation of these transporters. Ceftriaxone 84-95 solute carrier family 1 member 2 Rattus norvegicus 60-65 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. Ceftriaxone 73-84 solute carrier family 1 member 2 Rattus norvegicus 35-40 30590449-0 2019 Ceftriaxone Treatment Preserves Cortical Inhibitory Interneuron Function via Transient Salvage of GLT-1 in a Rat Traumatic Brain Injury Model. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 98-103 30590449-5 2019 Ceftriaxone, a beta-lactam antibiotic, is a potent stimulator of the expression of rodent GLT-1 and would presumably decrease excitotoxic damage to GABAergic interneurons. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 90-95 30590449-8 2019 We show that neocortical GLT-1 gene and protein expression are significantly reduced 1 week after TBI, and this transient loss is mitigated by ceftriaxone. Ceftriaxone 143-154 solute carrier family 1 member 2 Rattus norvegicus 25-30 30590449-11 2019 Our results highlight prospects for ceftriaxone as an intervention after TBI to prevent cortical inhibitory interneuron dysfunction, partly by preserving GLT-1 expression. Ceftriaxone 36-47 solute carrier family 1 member 2 Rattus norvegicus 154-159 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 47-52 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 92-115 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 117-122 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 13-16 solute carrier family 1 member 2 Rattus norvegicus 47-52 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 13-16 solute carrier family 1 member 2 Rattus norvegicus 92-115 31628912-3 2019 Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. Ceftriaxone 13-16 solute carrier family 1 member 2 Rattus norvegicus 117-122 31100299-10 2019 Moreover, repeated administrations of ceftriaxone during cocaine-free perios attenuated CPP persistence and normalized GLT-1 level in the NAc. Ceftriaxone 38-49 solute carrier family 1 member 2 Rattus norvegicus 119-124 31100299-12 2019 Additionally, we are the first to report that ceftriaxone strongly upregulates the GLT-1 in the HIP in a transcriptional mechanism involving the Nf-kappaB transcription factor. Ceftriaxone 46-57 solute carrier family 1 member 2 Rattus norvegicus 83-88 31019528-7 2019 Moreover, ceftriaxone can promote glutamate circulation and synaptic plasticity (all p < 0.05) by raising astroglial GLT-1 (p < 0.05) and then improve depressive behaviors of the CUMS-induced model rats (p < 0.05). Ceftriaxone 10-21 solute carrier family 1 member 2 Rattus norvegicus 117-122 29913736-0 2018 Effects of the excitatory amino acid transporter subtype 2 (EAAT-2) inducer ceftriaxone on different pain modalities in rat. Ceftriaxone 76-87 solute carrier family 1 member 2 Rattus norvegicus 60-66 29913736-4 2018 Ceftriaxone, a beta-lactam, induces EAAT-2 and has proven effect for the treatment of neuropathic pain. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 36-42 29913738-0 2018 Effects of the excitatory amino acid transporter subtype 2 (EAAT-2) transporter inducer ceftriaxone (an antibiotic) on different pain modalities in rat. Ceftriaxone 88-99 solute carrier family 1 member 2 Rattus norvegicus 60-66 28984398-8 2018 However, both clavulanic acid and ceftriaxone up-regulated GLT1 expression in rat cortical and human spinal astrocyte cultures. Ceftriaxone 34-45 solute carrier family 1 member 2 Rattus norvegicus 59-63 27796747-9 2017 We also found that the administration of beta-lactam antibiotic ceftriaxone increased glutamate transporter-1 protein expression and significantly reduced HI-induced WM injury in neonatal DEX-treated rats. Ceftriaxone 64-75 solute carrier family 1 member 2 Rattus norvegicus 86-109 28631864-4 2017 Initiation of a ceftriaxone regimen at the time of nigrostriatal lesion can attenuate tyrosine hydroxylase loss in conjunction with increased glutamate uptake and glutamate transporter GLT-1 expression in a rat 6-hydroxydopamine model. Ceftriaxone 16-27 solute carrier family 1 member 2 Rattus norvegicus 185-190 28631864-9 2017 The ceftriaxone-treated l-dopa group had significantly increased striatal GLT-1 expression and glutamate uptake. Ceftriaxone 4-15 solute carrier family 1 member 2 Rattus norvegicus 74-79 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. Ceftriaxone 69-80 solute carrier family 1 member 2 Rattus norvegicus 32-37 28495973-1 2017 Long-term treatment with ceftriaxone attenuates the reinstatement of cocaine seeking while increasing the function of the glutamate transporter 1 (GLT-1) and system xC- (Sxc) in the nucleus accumbens core (NAc). Ceftriaxone 25-36 solute carrier family 1 member 2 Rattus norvegicus 122-145 28495973-1 2017 Long-term treatment with ceftriaxone attenuates the reinstatement of cocaine seeking while increasing the function of the glutamate transporter 1 (GLT-1) and system xC- (Sxc) in the nucleus accumbens core (NAc). Ceftriaxone 25-36 solute carrier family 1 member 2 Rattus norvegicus 147-152 27932896-6 2016 Furthermore, repeated intrathecal administrations of ceftriaxone dose-dependently prevented the development of mechanical hyperalgesia and allodynia in ZDF rats, which were correlated with enhanced GLT-1 expression without altering the basal glutamate levels in the spinal cord of ZDF rats. Ceftriaxone 53-64 solute carrier family 1 member 2 Rattus norvegicus 198-203 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. Ceftriaxone 26-37 solute carrier family 1 member 2 Rattus norvegicus 201-206 27888396-4 2017 We also tested the effects of ceftriaxone (CEF), known to upregulate GLT-1, in animals administered EtOH and MA. Ceftriaxone 30-41 solute carrier family 1 member 2 Rattus norvegicus 69-74 27888396-4 2017 We also tested the effects of ceftriaxone (CEF), known to upregulate GLT-1, in animals administered EtOH and MA. Ceftriaxone 43-46 solute carrier family 1 member 2 Rattus norvegicus 69-74 27888396-13 2017 These findings demonstrated that sequential exposure to EtOH and MA has additive effect in downregulation of GLT-1 and this effect can be attenuated by CEF treatment. Ceftriaxone 152-155 solute carrier family 1 member 2 Rattus norvegicus 109-114 27932896-4 2016 Finally, the effects of repeated intrathecal injections of ceftriaxone, which was previously shown to enhance GLT-1 expression, on the development of mechanical allodynia and hyperalgesia as well as on basal extracellular level of glutamate and the expression of GLT-1 in the spinal cord of ZDF rats were evaluated. Ceftriaxone 59-70 solute carrier family 1 member 2 Rattus norvegicus 110-115 27558732-7 2016 Finally, ceftriaxone pretreatment (200mg/kg/day, 5days) before the 15min BCCAO prevented the development of PPD, and prevented the reduction of GLT-1 expression in the mPFC. Ceftriaxone 9-20 solute carrier family 1 member 2 Rattus norvegicus 144-149 27558732-8 2016 CONCLUSIONS: Taken together, our results suggested that ceftriaxone pretreatment before brain ischemia during pregnancy may reduce the propensity for the development of PPD by preventing the loss of GLT-1 expression in the mPFC. Ceftriaxone 56-67 solute carrier family 1 member 2 Rattus norvegicus 199-204 26037843-3 2015 The present study was carried out to investigate the effect of ceftriaxone (GLT-1 upregulator) and Brilliant Blue G (P2X7 antagonist) against PTZ-induced kindling in rats. Ceftriaxone 63-74 solute carrier family 1 member 2 Rattus norvegicus 76-81 27060486-0 2016 Effects of ceftriaxone on ethanol, nicotine or sucrose intake by alcohol-preferring (P) rats and its association with GLT-1 expression. Ceftriaxone 11-22 solute carrier family 1 member 2 Rattus norvegicus 118-123 27060486-2 2016 We have shown that administration of ceftriaxone (CEF), a beta-lactam antibiotic, reduced EtOH intake and increased glutamate transporter 1 (GLT-1) expression in mesocorticolimbic regions of male and female alcohol-preferring (P) rats. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 116-139 27060486-2 2016 We have shown that administration of ceftriaxone (CEF), a beta-lactam antibiotic, reduced EtOH intake and increased glutamate transporter 1 (GLT-1) expression in mesocorticolimbic regions of male and female alcohol-preferring (P) rats. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 141-146 27060486-2 2016 We have shown that administration of ceftriaxone (CEF), a beta-lactam antibiotic, reduced EtOH intake and increased glutamate transporter 1 (GLT-1) expression in mesocorticolimbic regions of male and female alcohol-preferring (P) rats. Ceftriaxone 50-53 solute carrier family 1 member 2 Rattus norvegicus 116-139 27060486-2 2016 We have shown that administration of ceftriaxone (CEF), a beta-lactam antibiotic, reduced EtOH intake and increased glutamate transporter 1 (GLT-1) expression in mesocorticolimbic regions of male and female alcohol-preferring (P) rats. Ceftriaxone 50-53 solute carrier family 1 member 2 Rattus norvegicus 141-146 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. Ceftriaxone 51-54 solute carrier family 1 member 2 Rattus norvegicus 141-146 26697981-8 2016 We also examined the influence of dihydrokainate (DHK) and ceftriaxone (CTX), which downregulate and upregulate Glt1, respectively, on pain development. Ceftriaxone 59-70 solute carrier family 1 member 2 Rattus norvegicus 112-116 26721358-0 2016 Ameliorative potential of pioglitazone and ceftriaxone alone and in combination in rat model of neuropathic pain: Targeting PPARgamma and GLT-1 pathways. Ceftriaxone 43-54 solute carrier family 1 member 2 Rattus norvegicus 138-143 26721358-2 2016 Present study has been designed to elucidate the interaction between the GLT-1 activator (ceftriaxone) and PPAR gamma agonist (pioglitazone) in the spinal nerve ligation induced neuropathic pain. Ceftriaxone 90-101 solute carrier family 1 member 2 Rattus norvegicus 73-78 26002627-10 2015 Blockade of GLT-1 by DHK reversed the effects of ceftriaxone on glutamate and implicated the role of GLT-1 in the normalization of extracellular glutamate by ceftriaxone. Ceftriaxone 158-169 solute carrier family 1 member 2 Rattus norvegicus 12-17 26002627-10 2015 Blockade of GLT-1 by DHK reversed the effects of ceftriaxone on glutamate and implicated the role of GLT-1 in the normalization of extracellular glutamate by ceftriaxone. Ceftriaxone 158-169 solute carrier family 1 member 2 Rattus norvegicus 101-106 26002627-13 2015 Our present study demonstrates that ceftriaxone treatment prevents ethanol drinking in part through normalization of extracellular glutamate concentrations in NAc of male P rats via GLT-1. Ceftriaxone 36-47 solute carrier family 1 member 2 Rattus norvegicus 182-187 26619231-11 2016 Glutamate transporter-1 (GLT-1) selective antagonist ceftriaxone prolonged CNS-OT latency, whereas GLT-1 selective inhibitor dihydrokainate shortened CNS-OT latency. Ceftriaxone 53-64 solute carrier family 1 member 2 Rattus norvegicus 0-23 26619231-11 2016 Glutamate transporter-1 (GLT-1) selective antagonist ceftriaxone prolonged CNS-OT latency, whereas GLT-1 selective inhibitor dihydrokainate shortened CNS-OT latency. Ceftriaxone 53-64 solute carrier family 1 member 2 Rattus norvegicus 25-30 26002627-0 2015 Ceftriaxone attenuates ethanol drinking and restores extracellular glutamate concentration through normalization of GLT-1 in nucleus accumbens of male alcohol-preferring rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 116-121 26002627-2 2015 We have previously reported that chronic ethanol-drinking downregulated glutamate transporter 1 (GLT-1) in nucleus accumbens (NAc) in male P rats in a manner that was reversed by ceftriaxone treatment. Ceftriaxone 179-190 solute carrier family 1 member 2 Rattus norvegicus 72-95 26002627-2 2015 We have previously reported that chronic ethanol-drinking downregulated glutamate transporter 1 (GLT-1) in nucleus accumbens (NAc) in male P rats in a manner that was reversed by ceftriaxone treatment. Ceftriaxone 179-190 solute carrier family 1 member 2 Rattus norvegicus 97-102 26002627-6 2015 In vivo microdialysis was performed to measure the extracellular glutamate concentrations in NAc and the effect of blockade of GLT-1 with dihydrokainic acid (DHK) on extracellular glutamate in NAc of ceftriaxone-treated rats was determined. Ceftriaxone 200-211 solute carrier family 1 member 2 Rattus norvegicus 127-132 26002627-10 2015 Blockade of GLT-1 by DHK reversed the effects of ceftriaxone on glutamate and implicated the role of GLT-1 in the normalization of extracellular glutamate by ceftriaxone. Ceftriaxone 49-60 solute carrier family 1 member 2 Rattus norvegicus 12-17 25806702-0 2015 Imaging in vivo glutamate fluctuations with [(11)C]ABP688: a GLT-1 challenge with ceftriaxone. Ceftriaxone 82-93 solute carrier family 1 member 2 Rattus norvegicus 61-66 25806702-3 2015 For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. Ceftriaxone 18-29 solute carrier family 1 member 2 Rattus norvegicus 80-85 25806702-3 2015 For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. Ceftriaxone 18-29 solute carrier family 1 member 2 Rattus norvegicus 99-104 25806702-3 2015 For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. Ceftriaxone 31-34 solute carrier family 1 member 2 Rattus norvegicus 80-85 25806702-3 2015 For this, we used ceftriaxone (CEF) administration in rats, an activator of the GLT-1 transporter (EAAT2), which is known to decrease extracellular levels of glutamate. Ceftriaxone 31-34 solute carrier family 1 member 2 Rattus norvegicus 99-104 26387186-5 2015 This sequence showed similar inhibition on the expression of GLT-la in sham and ceftriaxone (Cef)-treated rats. Ceftriaxone 80-91 solute carrier family 1 member 2 Rattus norvegicus 61-64 26387186-5 2015 This sequence showed similar inhibition on the expression of GLT-la in sham and ceftriaxone (Cef)-treated rats. Ceftriaxone 93-96 solute carrier family 1 member 2 Rattus norvegicus 61-64 25499022-2 2015 Ceftriaxone increases expression of glutamate transporter 1 (GLT-1) and affords neuroprotection. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 36-59 25499022-2 2015 Ceftriaxone increases expression of glutamate transporter 1 (GLT-1) and affords neuroprotection. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 61-66 25499022-9 2015 Increased GLT-1 expression and its co-localization with astrocytes were observed in the striatum and hippocampus in the ceftriaxone-treated animals. Ceftriaxone 120-131 solute carrier family 1 member 2 Rattus norvegicus 10-15 25499022-10 2015 To our knowledge, this is the first study showing a relationship between ceftriaxone-induced GLT-1 expression, neuroprotection, and improved cognition in a PD rat model. Ceftriaxone 73-84 solute carrier family 1 member 2 Rattus norvegicus 93-98 24650590-0 2014 Ceftriaxone, a GLT-1 transporter activator, disrupts hippocampal learning in rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 15-20 25270764-1 2015 Ceftriaxone(Cef) selectively increases the expression of glial glutamate transporter-1 (GLT-1), which was thought to be neuroprotective in some circumstances. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 57-93 25270764-12 2015 Ceftriaxone up-regulates GLT-1 expression and uptake of glutamate, diminishes the excitotoxicity of glutamate and then protects neurons against global brain ischemia. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 25-30 24687412-2 2014 We have recently demonstrated that ceftriaxone treatment induced upregulation of GLT1 levels and attenuated ethanol intake; however, less is known about the involvement of xCT on ethanol intake. Ceftriaxone 35-46 solute carrier family 1 member 2 Rattus norvegicus 81-85 24650590-3 2014 It has been shown that the beta-lactam antibiotic ceftriaxone (Rocephin) induces an up-regulation of the glutamate transporter GLT-1. Ceftriaxone 50-61 solute carrier family 1 member 2 Rattus norvegicus 127-132 24650590-3 2014 It has been shown that the beta-lactam antibiotic ceftriaxone (Rocephin) induces an up-regulation of the glutamate transporter GLT-1. Ceftriaxone 63-71 solute carrier family 1 member 2 Rattus norvegicus 127-132 24650590-11 2014 Our findings show that a potential up-regulation of GLT-1 via ceftriaxone administration has detrimental effects on spatial learning and memory in rats. Ceftriaxone 62-73 solute carrier family 1 member 2 Rattus norvegicus 52-57 24452391-9 2014 Finally, ceftriaxone treatment was associated with lasting upregulation of ethanol withdrawal-induced downregulation of EAAT2 in the striatum. Ceftriaxone 9-20 solute carrier family 1 member 2 Rattus norvegicus 120-125 24297323-3 2014 The beta-lactam antibiotic, ceftriaxone, increases the expression of glutamate transporter 1 (GLT-1), a glutamate transporter that plays a major role in glutamate clearance in central nervous system and may attenuate adverse behavioral or neurobiological function in other neurodegenerative disease models. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 69-92 24297323-3 2014 The beta-lactam antibiotic, ceftriaxone, increases the expression of glutamate transporter 1 (GLT-1), a glutamate transporter that plays a major role in glutamate clearance in central nervous system and may attenuate adverse behavioral or neurobiological function in other neurodegenerative disease models. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 94-99 24452391-0 2014 Attenuation of ethanol withdrawal by ceftriaxone-induced upregulation of glutamate transporter EAAT2. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 95-100 24452391-3 2014 Using a rat model of ethanol withdrawal, we tested whether ceftriaxone, a beta-lactam antibiotic known to increase the expression and activity of glutamate uptake transporter EAAT2, reduces the occurrence or severity of ethanol withdrawal manifestations. Ceftriaxone 59-70 solute carrier family 1 member 2 Rattus norvegicus 175-180 24631672-0 2014 Ceftriaxone alleviates early brain injury after subarachnoid hemorrhage by increasing excitatory amino acid transporter 2 expression via the PI3K/Akt/NF-kappaB signaling pathway. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 86-121 25146518-2 2014 METHODS: A beta-lactam antibiotic, ceftriaxone (CTX) was used to selectively induce transcription of the gene encoding GLT-1 and upregulate GLT-1 expression as an agonist. Ceftriaxone 35-46 solute carrier family 1 member 2 Rattus norvegicus 119-124 25146518-2 2014 METHODS: A beta-lactam antibiotic, ceftriaxone (CTX) was used to selectively induce transcription of the gene encoding GLT-1 and upregulate GLT-1 expression as an agonist. Ceftriaxone 35-46 solute carrier family 1 member 2 Rattus norvegicus 140-145 24631672-2 2014 The aim of this study was to explore the neuroprotective effect of ceftriaxone (CEF), a potent compound that up-regulates EAAT2, against EBI and the potential mechanisms using in vitro experiments and a rat model of SAH. Ceftriaxone 67-78 solute carrier family 1 member 2 Rattus norvegicus 122-127 24631672-2 2014 The aim of this study was to explore the neuroprotective effect of ceftriaxone (CEF), a potent compound that up-regulates EAAT2, against EBI and the potential mechanisms using in vitro experiments and a rat model of SAH. Ceftriaxone 80-83 solute carrier family 1 member 2 Rattus norvegicus 122-127 24741055-8 2014 Ceftriaxone-induced inhibition of reinstated heroin seeking was blocked by morpholino-antisense targeting GLT-1 synthesis. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 106-111 24277205-3 2014 The beta-lactam antibiotic ceftriaxone (CTX) has been reported to induce neuroprotection in animal models of diverse neurologic diseases via up-regulation of GLT-1. Ceftriaxone 27-38 solute carrier family 1 member 2 Rattus norvegicus 158-163 24071615-1 2014 BACKGROUND: The beta-lactam antibiotic ceftriaxone stimulates glutamate transporter GLT-1 expression and is effective in neuropathic and visceral pain models. Ceftriaxone 39-50 solute carrier family 1 member 2 Rattus norvegicus 84-89 24123246-0 2014 Upregulation of GLT-1 by treatment with ceftriaxone alleviates radicular pain by reducing spinal astrocyte activation and neuronal hyperexcitability. Ceftriaxone 40-51 solute carrier family 1 member 2 Rattus norvegicus 16-21 25028668-11 2014 CONCLUSION: Our results suggest that ceftriaxone, an upregulator/activator of GLT1, could concomitantly reduce oxidative stress and apoptosis and producing its new analogs lacking antimicrobial activity may represent a novel approach for neuropathic pain treatment. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 78-82 23985782-2 2014 In particular, compounds that increase expression of the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease measures of drug seeking. Ceftriaxone 118-129 solute carrier family 1 member 2 Rattus norvegicus 90-95 22998524-3 2013 In this study, GLT-1 up-regulation was induced by ceftriaxone, and L-glutamate was added to induce glutamate toxicity in primary cultured rat cortical cells. Ceftriaxone 50-61 solute carrier family 1 member 2 Rattus norvegicus 15-20 23893122-3 2013 We examined, then, whether ceftriaxone (CEF) would affect both GLT1 and ENT1 levels in these brain regions. Ceftriaxone 27-38 solute carrier family 1 member 2 Rattus norvegicus 63-67 23893122-3 2013 We examined, then, whether ceftriaxone (CEF) would affect both GLT1 and ENT1 levels in these brain regions. Ceftriaxone 40-43 solute carrier family 1 member 2 Rattus norvegicus 63-67 23893122-11 2013 These findings provide evidence for potential regulatory effects of CEF on both GLT1 and ENT1 expression in reducing ethanol intake. Ceftriaxone 68-71 solute carrier family 1 member 2 Rattus norvegicus 80-84 23638698-8 2013 Chronic treatment with ceftriaxone (200 mg kg(-1) i.p., once daily, 7 days), an EAAT2 expression enhancer, increased the actions of glutamate and DHK, suggesting a functional impact of EAAT2 up-regulation on the glutamatergic system. Ceftriaxone 23-34 solute carrier family 1 member 2 Rattus norvegicus 80-85 23638698-8 2013 Chronic treatment with ceftriaxone (200 mg kg(-1) i.p., once daily, 7 days), an EAAT2 expression enhancer, increased the actions of glutamate and DHK, suggesting a functional impact of EAAT2 up-regulation on the glutamatergic system. Ceftriaxone 23-34 solute carrier family 1 member 2 Rattus norvegicus 185-190 23523747-3 2013 Recently, a neuroprotective effect of preconditioning with a beta-lactam antibiotic ceftriaxone (CTX) that increases expression of GLT-1 has been reported in animal models of focal ischemia. Ceftriaxone 84-95 solute carrier family 1 member 2 Rattus norvegicus 131-136 23537837-2 2013 We recently reported that the administration of ceftriaxone (CEF), a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1) levels/activity, decreased the maintenance of EtOH intake in adult male alcohol-preferring (P) rats. Ceftriaxone 48-59 solute carrier family 1 member 2 Rattus norvegicus 112-135 23537837-2 2013 We recently reported that the administration of ceftriaxone (CEF), a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1) levels/activity, decreased the maintenance of EtOH intake in adult male alcohol-preferring (P) rats. Ceftriaxone 48-59 solute carrier family 1 member 2 Rattus norvegicus 137-141 23537837-2 2013 We recently reported that the administration of ceftriaxone (CEF), a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1) levels/activity, decreased the maintenance of EtOH intake in adult male alcohol-preferring (P) rats. Ceftriaxone 61-64 solute carrier family 1 member 2 Rattus norvegicus 112-135 23537837-2 2013 We recently reported that the administration of ceftriaxone (CEF), a beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1) levels/activity, decreased the maintenance of EtOH intake in adult male alcohol-preferring (P) rats. Ceftriaxone 61-64 solute carrier family 1 member 2 Rattus norvegicus 137-141 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. Ceftriaxone 210-221 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. Ceftriaxone 210-221 solute carrier family 1 member 2 Rattus norvegicus 277-281 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. Ceftriaxone 210-221 solute carrier family 1 member 2 Rattus norvegicus 277-281 23719800-7 2013 To localize the effects of GLT1 upregulation within NAc, we tested the hypothesis that blockade of GLT1 in NAc core, but not shell, would reverse the ceftriaxone-mediated effect. Ceftriaxone 150-161 solute carrier family 1 member 2 Rattus norvegicus 99-103 23719800-9 2013 Our results reveal that the ceftriaxone-mediated attenuation of cue-induced cocaine reinstatement is reversed by GLT1 blockade in core, but not shell, and further implicate core GLT1 as a potential therapeutic target for cocaine relapse. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 113-117 23719800-9 2013 Our results reveal that the ceftriaxone-mediated attenuation of cue-induced cocaine reinstatement is reversed by GLT1 blockade in core, but not shell, and further implicate core GLT1 as a potential therapeutic target for cocaine relapse. Ceftriaxone 28-39 solute carrier family 1 member 2 Rattus norvegicus 178-182 23594486-8 2013 We also found that the administration of beta-lactam antibiotic ceftriaxone increased GLT-1 protein expression and significantly reduced HI-induced brain injury in neonatal DEX-treated rats. Ceftriaxone 64-75 solute carrier family 1 member 2 Rattus norvegicus 86-91 23059796-1 2012 We have previously shown that ceftriaxone, beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1), reduced ethanol intake in alcohol-preferring (P) rats. Ceftriaxone 30-41 solute carrier family 1 member 2 Rattus norvegicus 86-109 23059796-1 2012 We have previously shown that ceftriaxone, beta-lactam antibiotic known to upregulate glutamate transporter 1 (GLT1), reduced ethanol intake in alcohol-preferring (P) rats. Ceftriaxone 30-41 solute carrier family 1 member 2 Rattus norvegicus 111-115 23893122-0 2013 Ceftriaxone treatment affects the levels of GLT1 and ENT1 as well as ethanol intake in alcohol-preferring rats. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 44-48 23510201-0 2013 Ceftriaxone treatment after traumatic brain injury restores expression of the glutamate transporter, GLT-1, reduces regional gliosis, and reduces post-traumatic seizures in the rat. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 101-106 23510201-3 2013 We tested, by immunoblot, in the rat lateral fluid percussion injury TBI model whether GLT-1 expression is depressed in the cortex after TBI, and whether GLT-1 expression after TBI is restored after treatment with ceftriaxone, a well-tolerated beta-lactam antibiotic previously shown to enhance GLT-1 expression in noninjured animals. Ceftriaxone 214-225 solute carrier family 1 member 2 Rattus norvegicus 154-159 23510201-3 2013 We tested, by immunoblot, in the rat lateral fluid percussion injury TBI model whether GLT-1 expression is depressed in the cortex after TBI, and whether GLT-1 expression after TBI is restored after treatment with ceftriaxone, a well-tolerated beta-lactam antibiotic previously shown to enhance GLT-1 expression in noninjured animals. Ceftriaxone 214-225 solute carrier family 1 member 2 Rattus norvegicus 154-159 23510201-6 2013 However, the loss of GLT-1 expression was reversed by treatment with ceftriaxone (200 mg/kg, daily, intraperitoneally). Ceftriaxone 69-80 solute carrier family 1 member 2 Rattus norvegicus 21-26 24409344-6 2013 We recently reported that treatment of alcohol-preferring rats with compounds ceftriaxone and GPI-1046, known to upregulate GLT1 levels, showed reduction in alcohol intake and attenuation of relapse-like ethanol-drinking behaviour. Ceftriaxone 78-89 solute carrier family 1 member 2 Rattus norvegicus 124-128 23047495-1 2013 PURPOSE: Ceftriaxone, a beta-lactam antibiotic, can selectively enhance the expression of glutamate transporter 1 (GLT1), the most abundant astrocytic glutamate transporter expressed in the cortex. Ceftriaxone 9-20 solute carrier family 1 member 2 Rattus norvegicus 90-113 23047495-1 2013 PURPOSE: Ceftriaxone, a beta-lactam antibiotic, can selectively enhance the expression of glutamate transporter 1 (GLT1), the most abundant astrocytic glutamate transporter expressed in the cortex. Ceftriaxone 9-20 solute carrier family 1 member 2 Rattus norvegicus 115-119 23047495-4 2013 In adult male rats, ceftriaxone (200 mg/kg) or vehicle was intraperitoneally injected daily for 5 days, a treatment regime previously established to upregulate GLT-1. Ceftriaxone 20-31 solute carrier family 1 member 2 Rattus norvegicus 160-165 22998524-4 2013 The results showed that up-regulated GLT-1 induced by 1 muM ceftriaxone for 2 days markedly increased cell viability, decreased apoptotic cell death and alleviated ultrastructural damage induced by 50 muM glutamate 15 min. Ceftriaxone 60-71 solute carrier family 1 member 2 Rattus norvegicus 37-42 22998524-9 2013 In conclusion, GLT-1 up-regulation induced by ceftriaxone plays a positive glutamate transporting role against glutamate toxicity in primary cultured rat cortical cells. Ceftriaxone 46-57 solute carrier family 1 member 2 Rattus norvegicus 15-20 23021150-9 2012 Treatment with the beta-lactam antibiotic ceftriaxone increased the expression of glutamate transporter 1 (Glt1) in the dorsal horn after SNI, raised transmitter uptake, and lowered extracellular glutamate. Ceftriaxone 42-53 solute carrier family 1 member 2 Rattus norvegicus 82-105 23021150-9 2012 Treatment with the beta-lactam antibiotic ceftriaxone increased the expression of glutamate transporter 1 (Glt1) in the dorsal horn after SNI, raised transmitter uptake, and lowered extracellular glutamate. Ceftriaxone 42-53 solute carrier family 1 member 2 Rattus norvegicus 107-111 22479544-2 2012 Recently, it has been demonstrated that ceftriaxone (CEF) robustly increases GLT-1 expression. Ceftriaxone 40-51 solute carrier family 1 member 2 Rattus norvegicus 77-82 22871519-3 2012 This investigation was designed to evaluate the interaction between co-administration of ceftriaxone, a specific GLT1 activator and minocycline, a specific microglia inhibitor, on the mechanical and cold allodynia of chronic constriction injury model (CCI) in rats. Ceftriaxone 89-100 solute carrier family 1 member 2 Rattus norvegicus 113-117 23054634-2 2012 Specifically, NMDAR antagonists such as MK-801, and an inducer of the expression of glutamate transporter subtype-1 (GLT-1) (ceftriaxone) are known to inhibit addictive behavior. Ceftriaxone 125-136 solute carrier family 1 member 2 Rattus norvegicus 84-115 23054634-2 2012 Specifically, NMDAR antagonists such as MK-801, and an inducer of the expression of glutamate transporter subtype-1 (GLT-1) (ceftriaxone) are known to inhibit addictive behavior. Ceftriaxone 125-136 solute carrier family 1 member 2 Rattus norvegicus 117-122 23054634-10 2012 CONCLUSION: The combined action of a low dose of an NMDAR antagonist (MK-801) and GLT-1 activation by ceftriaxone effectively changed different phases of CPP behavior. Ceftriaxone 102-113 solute carrier family 1 member 2 Rattus norvegicus 82-87 22521042-2 2012 Using reinstatement of conditioned place preference (CPP), we determined whether ceftriaxone, a beta-lactam antibiotic known to increase the expression and activity of the glutamate transporter (EAAT2) on glial cells, blocks methamphetamine-triggered reinstatement of CPP. Ceftriaxone 81-92 solute carrier family 1 member 2 Rattus norvegicus 195-200 22521042-7 2012 Using real time PCR, EAAT2 mRNA levels in the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) were quantified in response to ceftriaxone. Ceftriaxone 137-148 solute carrier family 1 member 2 Rattus norvegicus 21-26 22521042-8 2012 Ceftriaxone blocked methamphetamine-triggered reinstatement of CPP and significantly increased EAAT2 mRNA levels in the mPFC, with a trend towards significance in the NAc. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 95-100 22076500-1 2012 Several studies showed that the up-regulation of glial glutamate transporter-1 (GLT-1) participates in the acquisition of brain ischemic tolerance induced by cerebral ischemic preconditioning or ceftriaxone pretreatment in rats. Ceftriaxone 195-206 solute carrier family 1 member 2 Rattus norvegicus 49-85 22680643-6 2012 We and others have recently found that ceftriaxone, an FDA-approved drug known to elevate GLT1 expression, attenuates cue-induced cocaine relapse. Ceftriaxone 39-50 solute carrier family 1 member 2 Rattus norvegicus 90-94 22479544-2 2012 Recently, it has been demonstrated that ceftriaxone (CEF) robustly increases GLT-1 expression. Ceftriaxone 53-56 solute carrier family 1 member 2 Rattus norvegicus 77-82 21422004-15 2011 CONCLUSIONS: These results indicate that CEF effectively reduces ethanol intake, possibly through activation of GLT1, and may be a potential therapeutic drug for alcohol addiction treatment. Ceftriaxone 41-44 solute carrier family 1 member 2 Rattus norvegicus 112-116 21693777-0 2011 Ceftriaxone preconditioning confers neuroprotection in neonatal rats through glutamate transporter 1 upregulation. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 77-100 21693777-1 2011 OBJECTIVE: This study investigated the hypothesis that ceftriaxone preconditioning ameliorates brain damage in neonatal animals through glutamate transporter 1 (GLT-1) upregulation. Ceftriaxone 55-66 solute carrier family 1 member 2 Rattus norvegicus 136-159 21693777-1 2011 OBJECTIVE: This study investigated the hypothesis that ceftriaxone preconditioning ameliorates brain damage in neonatal animals through glutamate transporter 1 (GLT-1) upregulation. Ceftriaxone 55-66 solute carrier family 1 member 2 Rattus norvegicus 161-166 21693777-5 2011 RESULTS: Repeated ceftriaxone injections significantly increased GLT-1 mRNA and protein levels but not GLAST. Ceftriaxone 18-29 solute carrier family 1 member 2 Rattus norvegicus 65-70 21524862-0 2011 Glutamate transporter subtype 1 (GLT-1) activator ceftriaxone attenuates amphetamine-induced hyperactivity and behavioral sensitization in rats. Ceftriaxone 50-61 solute carrier family 1 member 2 Rattus norvegicus 0-38 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. Ceftriaxone 93-104 solute carrier family 1 member 2 Rattus norvegicus 43-81 21933448-5 2011 Compounds, such as ceftriaxone, that enhance the expression of GLT1 may exert neuroprotective effect in HIE. Ceftriaxone 19-30 solute carrier family 1 member 2 Rattus norvegicus 63-67 21933448-12 2011 GLT1 expression was observed in the cortical neurons of ceftriaxone treated rats. Ceftriaxone 56-67 solute carrier family 1 member 2 Rattus norvegicus 0-4 21256174-2 2011 Recent investigations suggest that ceftriaxone, a beta-lactam antibiotic, stimulates GLT-1 expression and confers neuroprotection against ischemic and motor neuron degeneration. Ceftriaxone 35-46 solute carrier family 1 member 2 Rattus norvegicus 85-90 21211547-11 2011 ), a selective GLT-1 transporter inhibitor, reversed the anti-allodynic and anti-hyperalgesic effects of ceftriaxone, at doses that produced no effect on its own. Ceftriaxone 105-116 solute carrier family 1 member 2 Rattus norvegicus 15-20 21846950-7 2011 RESULTS: Five-day treatment with 100 muM ceftriaxone significantly increased both GLAST and GLT-1 protein levels 31.3% and 47.5% above control, respectively, increased the Vmax 29.3%, increased the Km of glutamate uptake 117.9%, and reduced neuronal death 22.0% after a 1 mM glutamate challenge. Ceftriaxone 41-52 solute carrier family 1 member 2 Rattus norvegicus 92-97 21846950-2 2011 In the present study, the effects of ceftriaxone and (2R, 4R)-APDC (APDC) on the protein expression of GLAST and GLT-1, the rate of glutamate uptake, and neuroprotection were evaluated in a cell culture model of glutamate excitotoxicity. Ceftriaxone 37-48 solute carrier family 1 member 2 Rattus norvegicus 113-118 21846950-9 2011 CONCLUSIONS: Chronic treatment with ceftriaxone or APDC provided neuroprotection from glutamate excitotoxicity while increasing GLAST and GLT-1 protein levels and increasing glutamate uptake. Ceftriaxone 36-47 solute carrier family 1 member 2 Rattus norvegicus 138-143 19651762-3 2009 We show that up-regulation of the glutamate transporter GLT-1 by ceftriaxone severely impaired mGluR-dependent long-term depression (LTD), induced at rat mossy fibre (MF)-CA3 synapses by repetitive stimulation of afferent fibres. Ceftriaxone 65-76 solute carrier family 1 member 2 Rattus norvegicus 56-61 20022427-6 2010 To further determine whether the above anti-nociceptive effects of Cef are a result of the up-regulation of spinal GLT-1 expression and its function, we further observed the effects of intrathecal administration of Cef in the same model. Ceftriaxone 67-70 solute carrier family 1 member 2 Rattus norvegicus 115-120 20022427-7 2010 It was found that intrathecal administration of Cef led to the specific up-regulation of GLT-1 expression and glutamate uptake ((3)H-glutamate) in the spinal dorsal horn, and similar anti-nociceptive effects to those of intraperitoneal administration of Cef. Ceftriaxone 48-51 solute carrier family 1 member 2 Rattus norvegicus 89-94 20022427-8 2010 The above effects of intrathecal Cef administration were all significantly inhibited by intrathecal administration of GLT-1 antisense oligodeoxynucleotides (As-ODNs). Ceftriaxone 33-36 solute carrier family 1 member 2 Rattus norvegicus 118-123 20547213-6 2010 The present studies explored whether daily intrathecal treatment of rats with ceftriaxone, a beta-lactam antibiotic that upregulates GLT-1 expression, could prevent development of hyperalgesia and allodynia following repeated morphine, reverse pain arising from central or peripheral neuropathy, and reduce glial activation in these models. Ceftriaxone 78-89 solute carrier family 1 member 2 Rattus norvegicus 133-138 20072121-2 2010 Recently, it has been shown that ceftriaxone (CEF)-induced GLT-1 upregulation is associated with an impairment of the prepulse inhibition (PPI) of the startle reflex, a simple form of information processing that is reduced in schizophrenia, and determines a strong reduction in hippocampal metabotropic glutamate receptor (mGluR)2/3-dependent long-term depression. Ceftriaxone 33-44 solute carrier family 1 member 2 Rattus norvegicus 59-64 20072121-2 2010 Recently, it has been shown that ceftriaxone (CEF)-induced GLT-1 upregulation is associated with an impairment of the prepulse inhibition (PPI) of the startle reflex, a simple form of information processing that is reduced in schizophrenia, and determines a strong reduction in hippocampal metabotropic glutamate receptor (mGluR)2/3-dependent long-term depression. Ceftriaxone 46-49 solute carrier family 1 member 2 Rattus norvegicus 59-64 20072121-4 2010 We showed that administration of LY379268 (1 mg/kg) prevented PPI alterations associated with GLT-1 upregulation, suggesting that CEF-induced PPI impairment was mGluR2/3 dependent. Ceftriaxone 130-133 solute carrier family 1 member 2 Rattus norvegicus 94-99 20072121-5 2010 In addition, we showed that CEF-induced GLT-1 upregulaton did not alter the expression of mGluR2/3, and also that it occurred at sites of mGluR2/3 expression. Ceftriaxone 28-31 solute carrier family 1 member 2 Rattus norvegicus 40-45 20004063-2 2010 Identification of beta-lactam antibiotics as pharmaceuticals which activate GLT-1 transporters prompted us to hypothesize that repeated beta-lactam antibiotic (ceftriaxone) administration blocks development of tolerance to morphine antinociception through GLT-1 activation. Ceftriaxone 160-171 solute carrier family 1 member 2 Rattus norvegicus 76-81 20004063-2 2010 Identification of beta-lactam antibiotics as pharmaceuticals which activate GLT-1 transporters prompted us to hypothesize that repeated beta-lactam antibiotic (ceftriaxone) administration blocks development of tolerance to morphine antinociception through GLT-1 activation. Ceftriaxone 160-171 solute carrier family 1 member 2 Rattus norvegicus 256-261 19651762-7 2009 Furthermore, ceftriaxone-induced GLT-1 up-regulation significantly reduced the magnitude of LTP at MF-CA3 synapses but not at Schaffer collateral-CA1 synapses. Ceftriaxone 13-24 solute carrier family 1 member 2 Rattus norvegicus 33-38 19625514-6 2009 Immunoblotting confirmed that the ceftriaxone-induced blockade of cocaine relapse was associated with an increase in GLT1 expression in both PFC and NAcc. Ceftriaxone 34-45 solute carrier family 1 member 2 Rattus norvegicus 117-121 19806886-5 2009 Co-administration of ceftriaxone sodium with morphine attenuated morphine tolerance and up-regulated GLT-1 expression, and the MWT remained at high level after 6 days. Ceftriaxone 21-39 solute carrier family 1 member 2 Rattus norvegicus 101-106 18985735-2 2009 To do this, we studied PPI in rats treated with ceftriaxone (200 mg/kg/day for 8 days), an antibiotic that selectively enhances GLT-1 expression and activity. Ceftriaxone 48-59 solute carrier family 1 member 2 Rattus norvegicus 128-133 18985735-3 2009 We showed that ceftriaxone-induced GLT-1 upregulation is associated with impaired PPI of the startle, that this effect is reversed by dihydrokainate, a GLT-1 antagonist, that GLT-1 expression correlates negatively with PPI, and that PPI normalizes when GLT-1a levels return to baseline. Ceftriaxone 15-26 solute carrier family 1 member 2 Rattus norvegicus 35-40 18985735-3 2009 We showed that ceftriaxone-induced GLT-1 upregulation is associated with impaired PPI of the startle, that this effect is reversed by dihydrokainate, a GLT-1 antagonist, that GLT-1 expression correlates negatively with PPI, and that PPI normalizes when GLT-1a levels return to baseline. Ceftriaxone 15-26 solute carrier family 1 member 2 Rattus norvegicus 152-157 18985735-3 2009 We showed that ceftriaxone-induced GLT-1 upregulation is associated with impaired PPI of the startle, that this effect is reversed by dihydrokainate, a GLT-1 antagonist, that GLT-1 expression correlates negatively with PPI, and that PPI normalizes when GLT-1a levels return to baseline. Ceftriaxone 15-26 solute carrier family 1 member 2 Rattus norvegicus 152-157 18342307-1 2008 Ceftriaxone (a beta-lactam antibiotic) has recently been identified as having the rare ability to increase the expression and functional activity of the glutamate transporter subtype 1 (GLT-1) in rat spinal cord cultures. Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 153-191 17442809-7 2007 Upregulation of GLT-1 expression in astrocytes with ceftriaxone protected CA1 neurons from forebrain ischemia. Ceftriaxone 52-63 solute carrier family 1 member 2 Rattus norvegicus 16-21 19008722-1 2008 OBJECTIVE: Ceftriaxone has been reported to reduce neuronal damage in amyotrophic lateral sclerosis and in an in-vitro model of neuronal ischaemia through increased expression and activity of the glutamate transporter, GLT1. Ceftriaxone 11-22 solute carrier family 1 member 2 Rattus norvegicus 219-223 19008722-10 2008 Ceftriaxone did not increase GLT1 expression, but increased GLT1 activity (P < 0.05). Ceftriaxone 0-11 solute carrier family 1 member 2 Rattus norvegicus 60-64 17363173-3 2007 Nature 433:73-77] reported that beta-lactam antibiotics (including ceftriaxone, which easily crosses the blood-brain barrier) increase glutamate transporter 1 (GLT-1) expression and reduce cell death resulting from oxygen-glucose deprivation (OGD) in dissociated embryonic cortical cultures. Ceftriaxone 67-78 solute carrier family 1 member 2 Rattus norvegicus 135-158 17363173-3 2007 Nature 433:73-77] reported that beta-lactam antibiotics (including ceftriaxone, which easily crosses the blood-brain barrier) increase glutamate transporter 1 (GLT-1) expression and reduce cell death resulting from oxygen-glucose deprivation (OGD) in dissociated embryonic cortical cultures. Ceftriaxone 67-78 solute carrier family 1 member 2 Rattus norvegicus 160-165