PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 15657599-6 2005 After 1 d of withdrawal, stimulation of central amygdala ERK phosphorylation increased cocaine seeking. Cocaine 87-94 Eph receptor B1 Rattus norvegicus 57-60 16271798-0 2005 Cocaine induction of ERK proteins in dorsal striatum of Fischer rats. Cocaine 0-7 Eph receptor B1 Rattus norvegicus 21-24 16271798-2 2005 In this study, we show that a single cocaine administration induces ERK phosphorylation in the caudate/putamen of Fischer rats. Cocaine 37-44 Eph receptor B1 Rattus norvegicus 68-71 15657599-0 2005 Central amygdala ERK signaling pathway is critical to incubation of cocaine craving. Cocaine 68-75 Eph receptor B1 Rattus norvegicus 17-20 17439498-8 2007 Cocaine-induced ERK and CREB(S133) phosphorylation were dissociated in many brain regions and failed to develop either tolerance or sensitization with chronic administration. Cocaine 0-7 Eph receptor B1 Rattus norvegicus 16-19 16219028-6 2005 Using western blots and MAPK activity assays, we found that cocaine-induced phosphorylation and activation of ERK, but not of CaMKs II or IV or GluR1, was augmented in nucleus accumbens of cocaine-sensitized rats. Cocaine 60-67 Eph receptor B1 Rattus norvegicus 110-113 16219028-7 2005 Unilateral infusions of the MAPK kinase inhibitor U0126 into nucleus accumbens attenuated cocaine-induced ERK and CREB phosphorylation in cocaine-sensitized rats. Cocaine 90-97 Eph receptor B1 Rattus norvegicus 106-109 16219028-9 2005 Therefore, enhanced activation of ERK, but not PKA, enables and mediates cocaine-induced CREB phosphorylation in nucleus accumbens of rats that are sensitized by repeated cocaine administration outside their home cages. Cocaine 73-80 Eph receptor B1 Rattus norvegicus 34-37 16219028-9 2005 Therefore, enhanced activation of ERK, but not PKA, enables and mediates cocaine-induced CREB phosphorylation in nucleus accumbens of rats that are sensitized by repeated cocaine administration outside their home cages. Cocaine 171-178 Eph receptor B1 Rattus norvegicus 34-37 15657599-7 2005 Results suggest that the incubation of cocaine craving is mediated by time-dependent increases in the responsiveness of the central amygdala ERK pathway to cocaine cues. Cocaine 39-46 Eph receptor B1 Rattus norvegicus 141-144 15657599-7 2005 Results suggest that the incubation of cocaine craving is mediated by time-dependent increases in the responsiveness of the central amygdala ERK pathway to cocaine cues. Cocaine 156-163 Eph receptor B1 Rattus norvegicus 141-144 15470197-3 2004 We examined whether the mitogen-activated protein kinase-extracellular receptor kinase (ERK) pathway may be involved in mediating the serine 133 CREB phosphorylation in cardiac nuclei after perinatal cocaine exposure. Cocaine 200-207 Eph receptor B1 Rattus norvegicus 88-91 15365088-7 2005 Cocaine stimulated a transient increase in the p38 MAPK activity at a time point of 15 min but reduced the extracellular signal-regulated kinase (ERK) activity at 5 and 15 min in FRMCs. Cocaine 0-7 Eph receptor B1 Rattus norvegicus 107-144 15365088-7 2005 Cocaine stimulated a transient increase in the p38 MAPK activity at a time point of 15 min but reduced the extracellular signal-regulated kinase (ERK) activity at 5 and 15 min in FRMCs. Cocaine 0-7 Eph receptor B1 Rattus norvegicus 146-149 15470197-8 2004 We found that perinatal cocaine exposure increased both phospho-ERK and phospho-RSK expression, indicative of an increased activity of these two enzymes. Cocaine 24-31 Eph receptor B1 Rattus norvegicus 64-67 15470197-10 2004 Our results thus illustrate that the ERK-RSK pathway was active in the postnatal rat heart at 1 and 7 d of age and that this pathway may mediate the increase in myocardial CREB activation after perinatal cocaine exposure in the day 7 hearts. Cocaine 204-211 Eph receptor B1 Rattus norvegicus 37-40 8764658-0 1996 Regulation of ERK (extracellular signal regulated kinase), part of the neurotrophin signal transduction cascade, in the rat mesolimbic dopamine system by chronic exposure to morphine or cocaine. Cocaine 186-193 Eph receptor B1 Rattus norvegicus 14-17 8764658-11 1996 Together, these findings support a scheme whereby chronic, systemic administration of morphine or cocaine leads to a sustained increase in ERK phosphorylation state and activity in the VTA, which, in turn, contributes to drug-induced increases in TH, and perhaps other drug-induced adaptations, elicited selectively in this brain region. Cocaine 98-105 Eph receptor B1 Rattus norvegicus 139-142 8764658-0 1996 Regulation of ERK (extracellular signal regulated kinase), part of the neurotrophin signal transduction cascade, in the rat mesolimbic dopamine system by chronic exposure to morphine or cocaine. Cocaine 186-193 Eph receptor B1 Rattus norvegicus 19-56 28585567-0 2017 Role of Src Family Kinases in BDNF-Mediated Suppression of Cocaine-Seeking and Prevention of Cocaine-Induced ERK, GluN2A, and GluN2B Dephosphorylation in the Prelimbic Cortex. Cocaine 93-100 Eph receptor B1 Rattus norvegicus 109-112 35368299-3 2022 In this study, we compared ERK activation in the nucleus accumbens (NAc) after cocaine reward and after positive social interaction (SI) with a partner-reward in male rats. Cocaine 79-86 Eph receptor B1 Rattus norvegicus 27-30 32312805-6 2020 In the PFC, we also find that WIN preexposure blunts the typical mRNA response to cocaine and instead results in alternative splicing and chromatin accessibility events, involving genes such as Npas2 Moreover, preexposure to WIN enhances the effects of cocaine on protein phosphorylation, including ERK/MAPK-targets like gephyrin, and modulates the synaptic AMPAR/GluR composition both in the PFC and the nucleus accumbens (NAcc). Cocaine 253-260 Eph receptor B1 Rattus norvegicus 299-302 29354053-0 2017 Activation of Dopamine D1-D2 Receptor Complex Attenuates Cocaine Reward and Reinstatement of Cocaine-Seeking through Inhibition of DARPP-32, ERK, and DeltaFosB. Cocaine 57-64 Eph receptor B1 Rattus norvegicus 141-144 29354053-0 2017 Activation of Dopamine D1-D2 Receptor Complex Attenuates Cocaine Reward and Reinstatement of Cocaine-Seeking through Inhibition of DARPP-32, ERK, and DeltaFosB. Cocaine 93-100 Eph receptor B1 Rattus norvegicus 141-144 28349660-2 2018 Central to these adaptations is decreased phospho-extracellular signal-regulated kinase (p-ERK), which plays a key role in cocaine seeking. Cocaine 123-130 Eph receptor B1 Rattus norvegicus 91-94 28349660-3 2018 Normalizing ERK phosphorylation in the PrL cortex immediately after cocaine self-administration decreases subsequent cocaine seeking. Cocaine 68-75 Eph receptor B1 Rattus norvegicus 12-15 28349660-3 2018 Normalizing ERK phosphorylation in the PrL cortex immediately after cocaine self-administration decreases subsequent cocaine seeking. Cocaine 117-124 Eph receptor B1 Rattus norvegicus 12-15 28349660-7 2018 Moreover, an intra-PrL cortical TC-2153 microinfusion immediately after self-administration prevented the cocaine-induced decrease in p-ERK within the PrL cortex during early abstinence. Cocaine 106-113 Eph receptor B1 Rattus norvegicus 136-139 28349660-9 2018 These data indicate that the STEP-induced ERK dephosphorylation in the PrL cortex during early abstinence is a critical neuroadaptation that promotes relapse to cocaine seeking and that systemic versus intra-PrL cortical inhibition of STEP during early abstinence differentially suppresses cocaine seeking. Cocaine 161-168 Eph receptor B1 Rattus norvegicus 42-45 28349660-9 2018 These data indicate that the STEP-induced ERK dephosphorylation in the PrL cortex during early abstinence is a critical neuroadaptation that promotes relapse to cocaine seeking and that systemic versus intra-PrL cortical inhibition of STEP during early abstinence differentially suppresses cocaine seeking. Cocaine 290-297 Eph receptor B1 Rattus norvegicus 42-45 27494324-4 2016 Prenatal cocaine exposure reduces activity-dependent proBDNF and BDNF release and elevates BDNF affinity for TrkB leading to increased tyrosine-phosphorylated TrkB, heightened Phospholipase C-gamma1 and N-Shc/Shc recruitment and higher downstream PI3K and ERK activation in response to ex vivo BDNF. Cocaine 9-16 Eph receptor B1 Rattus norvegicus 256-259 25502299-0 2015 Differential effects of cocaine on extracellular signal-regulated kinase phosphorylation in nuclei of the extended amygdala and prefrontal cortex of psychogenetically selected Roman high- and low-avoidance rats. Cocaine 24-31 Eph receptor B1 Rattus norvegicus 35-72 25373870-2 2015 Within the mesocorticolimbic circuit, repeated cocaine administration activates extracellular signal-regulated kinase (ERK). Cocaine 47-54 Eph receptor B1 Rattus norvegicus 80-117 25373870-2 2015 Within the mesocorticolimbic circuit, repeated cocaine administration activates extracellular signal-regulated kinase (ERK). Cocaine 47-54 Eph receptor B1 Rattus norvegicus 119-122 25373870-11 2015 Inhibition of VTA ERK prior to each social defeat attenuated the development of stress-induced sensitization and prevented stress-induced enhancement of cocaine self-administration during a continuous access binge. Cocaine 153-160 Eph receptor B1 Rattus norvegicus 18-21 25373870-12 2015 CONCLUSIONS: These results suggest that enhanced activation of ERK in the VTA due to brief defeats is critical in the induction of sensitization and escalated cocaine taking. Cocaine 159-166 Eph receptor B1 Rattus norvegicus 63-66 26861675-9 2016 The ERK-CREB-Fos pathway and the NMDA receptor NR2B subunits in the NAc were involved in the cocaine-induced behavioral sensitization. Cocaine 93-100 Eph receptor B1 Rattus norvegicus 4-7 26398380-0 2015 Working memory deficits and alterations of ERK and CREB phosphorylation following withdrawal from cocaine self-administration. Cocaine 98-105 Eph receptor B1 Rattus norvegicus 43-46 26398380-11 2015 CONCLUSION: Our results suggest that cocaine self-administration results in cognitive impairments and alterations in ERK/CREB signaling pathway long after discontinuation of drug use. Cocaine 37-44 Eph receptor B1 Rattus norvegicus 117-120 25502299-3 2015 Cocaine induces short- and long-term neuronal plasticity via activation of the extracellular signal-regulated kinase (ERK) pathway. Cocaine 0-7 Eph receptor B1 Rattus norvegicus 79-116 25502299-3 2015 Cocaine induces short- and long-term neuronal plasticity via activation of the extracellular signal-regulated kinase (ERK) pathway. Cocaine 0-7 Eph receptor B1 Rattus norvegicus 118-121 25502299-4 2015 This study compares the effects of acute cocaine on ERK phosphorylation (pERK) in limbic brain areas of Roman rats. Cocaine 41-48 Eph receptor B1 Rattus norvegicus 52-55 25522720-7 2015 Nucleus Accumbens (NAc) phosphorylated ERK (pERK) levels were increased after re-exposure to the cocaine-paired, but not the saline-paired chamber, regardless of whether or not CPP behavior was expressed. Cocaine 97-104 Eph receptor B1 Rattus norvegicus 39-42 25522720-10 2015 Our results suggest that NAc ERK phosphorylation may be involved with retrieving the contextual information of a cocaine-association, without necessarily motivating the expression of CPP behavior. Cocaine 113-120 Eph receptor B1 Rattus norvegicus 29-32 24953280-8 2014 These results suggest that the phosphorylation of CREB by cocaine in the NAcc was blocked by the CART 55-102 peptide via the inhibition of D1R and D2R stimulation, D3R phosphorylation, cAMP/PKA signaling and ERK phosphorylated kinase signaling. Cocaine 58-65 Eph receptor B1 Rattus norvegicus 208-211 23665060-3 2013 We investigated whether ERK/CREB intracellular responses in the mesocorticolimbic circuitry underlying cocaine environmental associations are sexually dimorphic. Cocaine 103-110 Eph receptor B1 Rattus norvegicus 24-27 23624776-1 2013 RATIONALE: Dephosphorylation of extracellular signal-regulated kinase (ERK) and cyclic AMP response element binding protein (CREB) in the dorsomedial prefrontal cortex (dmPFC) at the end of short access (ShA) cocaine self-administration is implicated in cocaine seeking. Cocaine 209-216 Eph receptor B1 Rattus norvegicus 32-69 23624776-1 2013 RATIONALE: Dephosphorylation of extracellular signal-regulated kinase (ERK) and cyclic AMP response element binding protein (CREB) in the dorsomedial prefrontal cortex (dmPFC) at the end of short access (ShA) cocaine self-administration is implicated in cocaine seeking. Cocaine 209-216 Eph receptor B1 Rattus norvegicus 71-74 23624776-1 2013 RATIONALE: Dephosphorylation of extracellular signal-regulated kinase (ERK) and cyclic AMP response element binding protein (CREB) in the dorsomedial prefrontal cortex (dmPFC) at the end of short access (ShA) cocaine self-administration is implicated in cocaine seeking. Cocaine 254-261 Eph receptor B1 Rattus norvegicus 32-69 23624776-1 2013 RATIONALE: Dephosphorylation of extracellular signal-regulated kinase (ERK) and cyclic AMP response element binding protein (CREB) in the dorsomedial prefrontal cortex (dmPFC) at the end of short access (ShA) cocaine self-administration is implicated in cocaine seeking. Cocaine 254-261 Eph receptor B1 Rattus norvegicus 71-74 24948065-0 2014 The effect of active and passive intravenous cocaine administration on the extracellular signal-regulated kinase (ERK) activity in the rat brain. Cocaine 45-52 Eph receptor B1 Rattus norvegicus 75-112 24948065-0 2014 The effect of active and passive intravenous cocaine administration on the extracellular signal-regulated kinase (ERK) activity in the rat brain. Cocaine 45-52 Eph receptor B1 Rattus norvegicus 114-117 24948065-6 2014 Passive, repeated iv cocaine administration resulted in a 45% increase in ERK phosphorylation in the hippocampus while cocaine self-administration did not change brain ERK activity. Cocaine 21-28 Eph receptor B1 Rattus norvegicus 74-77 24948065-7 2014 On the 1st day of extinction, the activity of the ERK in the prefrontal cortex was decreased in rats with a history of cocaine chronic intake: by 66% for "active" cocaine group and by 35% for "yoked" cocaine group. Cocaine 119-126 Eph receptor B1 Rattus norvegicus 50-53 24948065-7 2014 On the 1st day of extinction, the activity of the ERK in the prefrontal cortex was decreased in rats with a history of cocaine chronic intake: by 66% for "active" cocaine group and by 35% for "yoked" cocaine group. Cocaine 163-170 Eph receptor B1 Rattus norvegicus 50-53 24948065-7 2014 On the 1st day of extinction, the activity of the ERK in the prefrontal cortex was decreased in rats with a history of cocaine chronic intake: by 66% for "active" cocaine group and by 35% for "yoked" cocaine group. Cocaine 163-170 Eph receptor B1 Rattus norvegicus 50-53 24948065-8 2014 On the 3rd day the reduction in the ERK activity (25-34%) was observed in the hippocampus for both cocaine-treated groups, and also in the nucleus accumbens for "yoked" cocaine group (40%). Cocaine 99-106 Eph receptor B1 Rattus norvegicus 36-39 24948065-8 2014 On the 3rd day the reduction in the ERK activity (25-34%) was observed in the hippocampus for both cocaine-treated groups, and also in the nucleus accumbens for "yoked" cocaine group (40%). Cocaine 169-176 Eph receptor B1 Rattus norvegicus 36-39 24948065-10 2014 Our findings suggest that cortical ERK is involved in cocaine seeking behavior in rats. Cocaine 54-61 Eph receptor B1 Rattus norvegicus 35-38 23232446-0 2013 Extracellular signal-regulated kinase in the basolateral amygdala, but not the nucleus accumbens core, is critical for context-response-cocaine memory reconsolidation in rats. Cocaine 136-143 Eph receptor B1 Rattus norvegicus 0-37 23232446-3 2013 Here, we used a rodent model of drug context-elicited relapse to test the hypothesis that ERK would be similarly required for the reconsolidation of context-response-cocaine memories that underlie drug context-induced reinstatement of instrumental cocaine-seeking behavior, with a focus on the NACc and on the basolateral amygdala (BLA), another important locus for the reconsolidation of cocaine memories. Cocaine 166-173 Eph receptor B1 Rattus norvegicus 90-93 23232446-3 2013 Here, we used a rodent model of drug context-elicited relapse to test the hypothesis that ERK would be similarly required for the reconsolidation of context-response-cocaine memories that underlie drug context-induced reinstatement of instrumental cocaine-seeking behavior, with a focus on the NACc and on the basolateral amygdala (BLA), another important locus for the reconsolidation of cocaine memories. Cocaine 248-255 Eph receptor B1 Rattus norvegicus 90-93 23232446-7 2013 These findings demonstrate that ERK activation in the BLA, but not the NACc, is required for the reconsolidation of context-response-cocaine associative memories. Cocaine 133-140 Eph receptor B1 Rattus norvegicus 32-35 23266327-3 2013 Considering that activation of the extracellular signal-regulated protein kinase (ERK) is suggested to be involved in cocaine-induced behavioral sensitization, we study the effects of perinatal protein deprivation on phosphorylated ERK2 (pERK2) protein levels in the NAc (core and shell) during different drug-free withdrawal periods. Cocaine 118-125 Eph receptor B1 Rattus norvegicus 35-80 23266327-3 2013 Considering that activation of the extracellular signal-regulated protein kinase (ERK) is suggested to be involved in cocaine-induced behavioral sensitization, we study the effects of perinatal protein deprivation on phosphorylated ERK2 (pERK2) protein levels in the NAc (core and shell) during different drug-free withdrawal periods. Cocaine 118-125 Eph receptor B1 Rattus norvegicus 82-85 23266327-7 2013 In the NAc core, cocaine induced ERK signaling pathway activation in a dose-dependent manner, and only D-rats showed a significant increase in pERK2 protein levels with the lowest dose of cocaine (5 mg/kg). Cocaine 17-24 Eph receptor B1 Rattus norvegicus 33-36 22359477-7 2011 These results indicate that ERK activation in the NAcc is necessary for the expression of cocaine-induced behavioral sensitization, and further suggest that repeated cocaine evokes neuronal plasticity involving ERK pathway in this site leading to long-lasting behavioral changes. Cocaine 166-173 Eph receptor B1 Rattus norvegicus 28-31 22359477-0 2011 Blockade of ERK Phosphorylation in the Nucleus Accumbens Inhibits the Expression of Cocaine-induced Behavioral Sensitization in Rats. Cocaine 84-91 Eph receptor B1 Rattus norvegicus 12-15 22359477-4 2011 In this study we demonstrate that blockade of ERK phosphorylation in the NAcc by a single bilateral microinjections of PD98059 (0.5 or 2.0micro g/side), or U0126 (0.1 or 1.0microg/side), into this site dose-dependently inhibited the expression of cocaine-induced behavioral sensitization when measured at day 7 following 6 consecutive daily cocaine injections (15 mg/kg, i.p.). Cocaine 247-254 Eph receptor B1 Rattus norvegicus 46-49 22359477-4 2011 In this study we demonstrate that blockade of ERK phosphorylation in the NAcc by a single bilateral microinjections of PD98059 (0.5 or 2.0micro g/side), or U0126 (0.1 or 1.0microg/side), into this site dose-dependently inhibited the expression of cocaine-induced behavioral sensitization when measured at day 7 following 6 consecutive daily cocaine injections (15 mg/kg, i.p.). Cocaine 341-348 Eph receptor B1 Rattus norvegicus 46-49 22359477-6 2011 Further, microinjection of PD98059 (2.0micro g/side) in the NAcc specifically lowered cocaine-induced increase of ERK phosphorylation levels in this site, while unaffecting p-38 protein levels. Cocaine 86-93 Eph receptor B1 Rattus norvegicus 114-117 22359477-7 2011 These results indicate that ERK activation in the NAcc is necessary for the expression of cocaine-induced behavioral sensitization, and further suggest that repeated cocaine evokes neuronal plasticity involving ERK pathway in this site leading to long-lasting behavioral changes. Cocaine 90-97 Eph receptor B1 Rattus norvegicus 28-31 22359477-7 2011 These results indicate that ERK activation in the NAcc is necessary for the expression of cocaine-induced behavioral sensitization, and further suggest that repeated cocaine evokes neuronal plasticity involving ERK pathway in this site leading to long-lasting behavioral changes. Cocaine 90-97 Eph receptor B1 Rattus norvegicus 211-214 22359477-7 2011 These results indicate that ERK activation in the NAcc is necessary for the expression of cocaine-induced behavioral sensitization, and further suggest that repeated cocaine evokes neuronal plasticity involving ERK pathway in this site leading to long-lasting behavioral changes. Cocaine 166-173 Eph receptor B1 Rattus norvegicus 211-214 21813685-0 2011 Extracellular signal-regulated kinase signaling in the ventral tegmental area mediates cocaine-induced synaptic plasticity and rewarding effects. Cocaine 87-94 Eph receptor B1 Rattus norvegicus 0-37 21813685-5 2011 We tested the hypothesis that VTA ERK activity is required for I-LTD and cocaine-induced long-term synaptic plasticity and behavioral effects. Cocaine 73-80 Eph receptor B1 Rattus norvegicus 34-37 21813685-6 2011 We show that the activation of receptors required for I-LTD increased ERK1/2 phosphorylation and inhibitors of ERK activation blocked I-LTD. We further demonstrate that ERK mediates cocaine-induced reduction of GABAergic inhibition and facilitation of LTP induction. Cocaine 182-189 Eph receptor B1 Rattus norvegicus 70-73 21813685-6 2011 We show that the activation of receptors required for I-LTD increased ERK1/2 phosphorylation and inhibitors of ERK activation blocked I-LTD. We further demonstrate that ERK mediates cocaine-induced reduction of GABAergic inhibition and facilitation of LTP induction. Cocaine 182-189 Eph receptor B1 Rattus norvegicus 111-114 21813685-7 2011 Finally, we show that cocaine conditioned place preference (CPP) training (15 mg/kg; four pairings) increased ERK1/2 phosphorylation in the VTA, while bilateral intra-VTA injections of a CB(1) antagonist or an inhibitor of ERK activation attenuated ERK1/2 phosphorylation and the acquisition, but not the expression, of CPP to cocaine. Cocaine 22-29 Eph receptor B1 Rattus norvegicus 110-113 21813685-8 2011 Our study has identified the CB(1) and ERK signaling cascade as a key mediator of several forms of cocaine-induced synaptic plasticity and provided evidence linking long-term synaptic plasticity in the VTA to rewarding effects of cocaine. Cocaine 99-106 Eph receptor B1 Rattus norvegicus 39-42 21813685-8 2011 Our study has identified the CB(1) and ERK signaling cascade as a key mediator of several forms of cocaine-induced synaptic plasticity and provided evidence linking long-term synaptic plasticity in the VTA to rewarding effects of cocaine. Cocaine 230-237 Eph receptor B1 Rattus norvegicus 39-42 21309958-0 2011 Emergence of context-associated GluR(1) and ERK phosphorylation in the nucleus accumbens core during withdrawal from cocaine self-administration. Cocaine 117-124 Eph receptor B1 Rattus norvegicus 44-47 21248106-6 2011 Vehicle-infused rats with a cocaine SA history showed significant decreases in ERK and cyclic AMP response element binding protein (CREB), but not Akt, phosphorylation after the final cocaine SA session that were reversed by intra-dmPFC BDNF. Cocaine 28-35 Eph receptor B1 Rattus norvegicus 79-82 21295078-2 2011 Several lines of evidence have shown that cAMP-response element binding protein (CREB), extracellular signal-regulated kinase (ERK), and c-fos have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol. Cocaine 213-220 Eph receptor B1 Rattus norvegicus 88-125 21295078-2 2011 Several lines of evidence have shown that cAMP-response element binding protein (CREB), extracellular signal-regulated kinase (ERK), and c-fos have pivotal role in CPP induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol. Cocaine 213-220 Eph receptor B1 Rattus norvegicus 127-130 21248106-8 2011 This study elucidates a mechanism whereby BDNF/TrkB (tropomyosin receptor kinase B) activates ERK-regulated CREB phosphorylation in the dmPFC to counteract the neuroadaptations induced by cocaine SA and subsequent relapse to cocaine-seeking. Cocaine 188-195 Eph receptor B1 Rattus norvegicus 94-97 21248106-7 2011 Additionally, BDNF"s ability to normalize cocaine-mediated decreases in ERK and CREB phosphorylation was blocked by U0126, demonstrating that ERK/MAPK activation mediated the behavioral effects. Cocaine 42-49 Eph receptor B1 Rattus norvegicus 72-75 21248106-7 2011 Additionally, BDNF"s ability to normalize cocaine-mediated decreases in ERK and CREB phosphorylation was blocked by U0126, demonstrating that ERK/MAPK activation mediated the behavioral effects. Cocaine 42-49 Eph receptor B1 Rattus norvegicus 142-145 19912338-0 2009 Context-specific modulation of cocaine-induced locomotor sensitization and ERK and CREB phosphorylation in the rat nucleus accumbens. Cocaine 31-38 Eph receptor B1 Rattus norvegicus 75-78 19912338-10 2009 Context-specific phosphorylation of ERK and CREB in the present study suggests that this signal transduction pathway is selectively activated in the same set of cocaine-activated accumbens neurons that mediate this learned association. Cocaine 161-168 Eph receptor B1 Rattus norvegicus 36-39 17610912-0 2007 Microinjection of CART peptide 55-102 into the nucleus accumbens blocks both the expression of behavioral sensitization and ERK phosphorylation by cocaine. Cocaine 147-154 Eph receptor B1 Rattus norvegicus 124-127 18359158-1 2008 Extracellular signal-regulated kinase (ERK) has been implicated in cocaine-induced behavioral sensitization. Cocaine 67-74 Eph receptor B1 Rattus norvegicus 0-37 18359158-1 2008 Extracellular signal-regulated kinase (ERK) has been implicated in cocaine-induced behavioral sensitization. Cocaine 67-74 Eph receptor B1 Rattus norvegicus 39-42 18359158-2 2008 We sought to determine whether ERK activation in the nucleus accumbens (NAcc), the site mediating the expression of behavioral sensitization, shows time-dependent changes after cocaine withdrawals. Cocaine 177-184 Eph receptor B1 Rattus norvegicus 31-34 18359158-3 2008 The basal levels of ERK phosphorylation in the NAcc show no changes on withdrawal day 1, while they increase on day 7, then gradually lower down to reach the same level on day 21 in cocaine compared to saline pre-exposed rats. Cocaine 182-189 Eph receptor B1 Rattus norvegicus 20-23 17898233-6 2007 In sensitized rats, ERK phosphorylation in the NAc increased during withdrawal and normalized after cocaine challenge. Cocaine 100-107 Eph receptor B1 Rattus norvegicus 20-23 18822274-2 2008 In this study, we show that a single cocaine administration (30 mg/kg) time-dependently increases ERK phosphorylation, c-Fos and FosB protein expression, and MKP-1 phosphorylation (p-MKP-1), in the caudate-putamen (CPu) and nucleus accumbens (NAc) of Fischer rats. Cocaine 37-44 Eph receptor B1 Rattus norvegicus 98-101 18822274-7 2008 Our data suggest that cocaine may modulate ERK pathway signaling through the activation of DA-D1 and NMDA receptors, subsequently influencing the IEG protein expression. Cocaine 22-29 Eph receptor B1 Rattus norvegicus 43-46 17920048-0 2007 Effects of acute cocaine on ERK and DARPP-32 phosphorylation pathways in the caudate-putamen of Fischer rats. Cocaine 17-24 Eph receptor B1 Rattus norvegicus 28-31 17920048-3 2007 A single cocaine administration (30 mg/kg) increased ERK-mediated signaling proteins, phosphoryation of cAMP response element-binding protein (CREB) kinase, pp90 ribosomal S6 kinase (RSK), and c-Fos protein levels in the caudate/putamen of Fischer rats. Cocaine 9-16 Eph receptor B1 Rattus norvegicus 53-56 17920048-5 2007 The phosphorylation states of these inhibitors of ERK and DARPP-32 proteins may thus contribute to the effects of cocaine on ERK- and DARPP-32-mediated cascades, on gene expression and on behaviors. Cocaine 114-121 Eph receptor B1 Rattus norvegicus 50-53 17920048-5 2007 The phosphorylation states of these inhibitors of ERK and DARPP-32 proteins may thus contribute to the effects of cocaine on ERK- and DARPP-32-mediated cascades, on gene expression and on behaviors. Cocaine 114-121 Eph receptor B1 Rattus norvegicus 125-128