PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25522720-9 2015 Conversely, the higher cocaine dose, independent of environment, resulted in increased NAc FosB, DeltaFosB and phosphorylated CREB (pCREB) protein levels compared to those conditioned with 5mg/kg cocaine (non-CPP-expressing). Cocaine 23-30 cAMP responsive element binding protein 1 Rattus norvegicus 126-130 34625609-7 2021 We also demonstrate a decrease in NF-kappaB activity, as well as in the expression of the active form of CREB, confirming the role of these transcription factors in the cocaine-induced memory impairment. Cocaine 169-176 cAMP responsive element binding protein 1 Rattus norvegicus 105-109 28923416-8 2017 In the presence of cocaine (100nM), the potency of quinpirole to inhibit the CREB signal was restored. Cocaine 19-26 cAMP responsive element binding protein 1 Rattus norvegicus 77-81 27053349-2 2017 In addition, several lines of study have indicated that cAMP response element-binding protein (CREB) and c-fos have important role in morphine-induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol. Cocaine 231-238 cAMP responsive element binding protein 1 Rattus norvegicus 56-93 27053349-2 2017 In addition, several lines of study have indicated that cAMP response element-binding protein (CREB) and c-fos have important role in morphine-induced conditioned place preference (CPP) induced by drugs of abuse, such as morphine, cocaine, nicotine, and alcohol. Cocaine 231-238 cAMP responsive element binding protein 1 Rattus norvegicus 95-99 26740398-7 2016 Specifically, opiates in several CNS regions including NAc, and cocaine more selectively in NAc, induce expression of certain adenylyl cyclase isoforms and PKA subunits via the transcription factor, CREB, and these transcriptional adaptations serve a homeostatic function to oppose drug action. Cocaine 64-71 cAMP responsive element binding protein 1 Rattus norvegicus 199-203 25716852-2 2015 However, overexpression of CREB, which increases excitability of AcbSh neurons, enhances cocaine-seeking behavior while producing depression-like behavior in tests of mood. Cocaine 89-96 cAMP responsive element binding protein 1 Rattus norvegicus 27-31 27261631-8 2016 Re-exposure to the cocaine context triggered cocaine seeking and increase in phosphorylation of cellular PKC substrates, including phospho-ERK and phospho-CREB. Cocaine 19-26 cAMP responsive element binding protein 1 Rattus norvegicus 155-159 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 cAMP responsive element binding protein 1 Rattus norvegicus 8-12 26398380-0 2015 Working memory deficits and alterations of ERK and CREB phosphorylation following withdrawal from cocaine self-administration. Cocaine 98-105 cAMP responsive element binding protein 1 Rattus norvegicus 51-55 26398380-8 2015 Upon T-maze training and 8-week withdrawal, cocaine-pretreated rats had higher levels of p-CREB/CREB in prefrontal cortex and dorsal striatum and lower in hippocampus compared to saline rats. Cocaine 44-51 cAMP responsive element binding protein 1 Rattus norvegicus 91-95 26398380-8 2015 Upon T-maze training and 8-week withdrawal, cocaine-pretreated rats had higher levels of p-CREB/CREB in prefrontal cortex and dorsal striatum and lower in hippocampus compared to saline rats. Cocaine 44-51 cAMP responsive element binding protein 1 Rattus norvegicus 96-100 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 cAMP responsive element binding protein 1 Rattus norvegicus 121-125 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 cAMP responsive element binding protein 1 Rattus norvegicus 50-54 23624776-10 2013 CONCLUSIONS: Activation of phospho-STEP may underlie ERK and CREB dephosphorylation in the dmPFC as well as internalization and degradation of GluN complexes during early withdrawal from both ShA and LgA cocaine self-administration, whereas differential alteration of AMPA receptor subunits after ShA and LgA cocaine self-administration depends on cocaine intake. Cocaine 309-316 cAMP responsive element binding protein 1 Rattus norvegicus 61-65 25100957-5 2014 Further, cocaine regulates proteins related to ERK, CREB and AKT signaling. Cocaine 9-16 cAMP responsive element binding protein 1 Rattus norvegicus 52-56 24560901-6 2014 Moreover, CART peptides were also found to block cocaine (1muM)-induced Ca(2+) influx, CaMKIIalpha phosphorylation, CaMKIIalpha-D3R interaction, and CREB phosphorylation. Cocaine 49-56 cAMP responsive element binding protein 1 Rattus norvegicus 149-153 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 cAMP responsive element binding protein 1 Rattus norvegicus 125-129 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 cAMP responsive element binding protein 1 Rattus norvegicus 125-129 23624776-10 2013 CONCLUSIONS: Activation of phospho-STEP may underlie ERK and CREB dephosphorylation in the dmPFC as well as internalization and degradation of GluN complexes during early withdrawal from both ShA and LgA cocaine self-administration, whereas differential alteration of AMPA receptor subunits after ShA and LgA cocaine self-administration depends on cocaine intake. Cocaine 204-211 cAMP responsive element binding protein 1 Rattus norvegicus 61-65 23624776-10 2013 CONCLUSIONS: Activation of phospho-STEP may underlie ERK and CREB dephosphorylation in the dmPFC as well as internalization and degradation of GluN complexes during early withdrawal from both ShA and LgA cocaine self-administration, whereas differential alteration of AMPA receptor subunits after ShA and LgA cocaine self-administration depends on cocaine intake. Cocaine 309-316 cAMP responsive element binding protein 1 Rattus norvegicus 61-65 23717324-12 2013 The concerted actions of miR-212 on striatal CREB and MeCP2/BDNF activity greatly attenuate the motivational effects of cocaine. Cocaine 120-127 cAMP responsive element binding protein 1 Rattus norvegicus 45-49 23665060-3 2013 We investigated whether ERK/CREB intracellular responses in the mesocorticolimbic circuitry underlying cocaine environmental associations are sexually dimorphic. Cocaine 103-110 cAMP responsive element binding protein 1 Rattus norvegicus 28-32 23665060-9 2013 CPP scores were positively correlated to NAc pERK, HIP pERK and CPu FosB protein levels, suggesting that similar to males, the ERK/CREB intracellular pathway in mesocorticolimbic regions undergoes cocaine induced neuroplasticity in female rats. Cocaine 197-204 cAMP responsive element binding protein 1 Rattus norvegicus 131-135 22453546-3 2012 OBJECTIVE: This study was conducted to investigate the effects of acupuncture on footshock-induced reinstatement of cocaine-seeking and the expression of c-Fos and the transcription factor cAMP response element-binding protein (CREB) in the NAc, used as markers of neuronal activation in conditions of stress-induced reinstatement to cocaine. Cocaine 334-341 cAMP responsive element binding protein 1 Rattus norvegicus 189-226 22453546-3 2012 OBJECTIVE: This study was conducted to investigate the effects of acupuncture on footshock-induced reinstatement of cocaine-seeking and the expression of c-Fos and the transcription factor cAMP response element-binding protein (CREB) in the NAc, used as markers of neuronal activation in conditions of stress-induced reinstatement to cocaine. Cocaine 334-341 cAMP responsive element binding protein 1 Rattus norvegicus 228-232 22453546-6 2012 RESULTS AND CONCLUSIONS: Acute footshock stress reinstated cocaine-seeking behavior and enhanced c-Fos expression and phosphorylated CREB (pCREB) activation in the NAc shell in cocaine pre-exposed rats. Cocaine 177-184 cAMP responsive element binding protein 1 Rattus norvegicus 133-137 22072694-5 2011 CREB enhanced cocaine reinforcement when expressed either throughout acquisition of self-administration or when expression was limited to postacquisition tests, indicating a direct effect of CREB independent of reinforcement-related learning. Cocaine 14-21 cAMP responsive element binding protein 1 Rattus norvegicus 0-4 21812869-0 2012 Chronic cocaine self-administration modulates ERK1/2 and CREB responses to dopamine receptor agonists in striatal slices. Cocaine 8-15 cAMP responsive element binding protein 1 Rattus norvegicus 57-61 21812869-2 2012 We hypothesized that chronic cocaine self-administration could influence dopamine D1 and D2 receptor activation of extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) and cyclic adenosine monophosphate response element-binding protein (CREB) phosphorylation. Cocaine 29-36 cAMP responsive element binding protein 1 Rattus norvegicus 247-251 21812869-6 2012 Cocaine self-administration also reduced D1R agonist-induced CREB phosphorylation in striatal slices, suggesting a downregulation of D1R signaling. Cocaine 0-7 cAMP responsive element binding protein 1 Rattus norvegicus 61-65 21812869-8 2012 In contrast, surprisingly, cocaine self-administration strongly potentiated D2R agonist-induced CREB phosphorylation selectively in the NAc portion of the slices. Cocaine 27-34 cAMP responsive element binding protein 1 Rattus norvegicus 96-100 21812869-10 2012 Our finding that selected cellular D2R responses to CREB were strengthened by cocaine self-administration could be relevant to understand how dopaminergic receptors participate in cocaine-induced behaviors. Cocaine 78-85 cAMP responsive element binding protein 1 Rattus norvegicus 52-56 21812869-10 2012 Our finding that selected cellular D2R responses to CREB were strengthened by cocaine self-administration could be relevant to understand how dopaminergic receptors participate in cocaine-induced behaviors. Cocaine 180-187 cAMP responsive element binding protein 1 Rattus norvegicus 52-56 22072694-0 2011 Overexpression of CREB in the nucleus accumbens shell increases cocaine reinforcement in self-administering rats. Cocaine 64-71 cAMP responsive element binding protein 1 Rattus norvegicus 18-22 22072694-1 2011 Chronic exposure to addictive drugs enhances cAMP response element binding protein (CREB)-regulated gene expression in nucleus accumbens (NAc), and these effects are thought to reduce the positive hedonic effects of passive cocaine administration. Cocaine 224-231 cAMP responsive element binding protein 1 Rattus norvegicus 45-82 22072694-1 2011 Chronic exposure to addictive drugs enhances cAMP response element binding protein (CREB)-regulated gene expression in nucleus accumbens (NAc), and these effects are thought to reduce the positive hedonic effects of passive cocaine administration. Cocaine 224-231 cAMP responsive element binding protein 1 Rattus norvegicus 84-88 22072694-2 2011 Here, we used viral-mediated gene transfer to produce short- and long-term regulation of CREB activity in NAc shell of rats engaging in volitional cocaine self-administration. Cocaine 147-154 cAMP responsive element binding protein 1 Rattus norvegicus 89-93 22072694-3 2011 Increasing CREB expression in NAc shell markedly enhanced cocaine reinforcement of self-administration behavior, as indicated by leftward (long-term) and upward (short-term) shifts in fixed ratio dose-response curves. Cocaine 58-65 cAMP responsive element binding protein 1 Rattus norvegicus 11-15 22072694-4 2011 CREB also increased the effort exerted by rats to obtain cocaine on more demanding progressive ratio schedules, an effect highly correlated with viral-induced modulation of BDNF protein in the NAc shell. Cocaine 57-64 cAMP responsive element binding protein 1 Rattus norvegicus 0-4 22072694-6 2011 Downregulating endogenous CREB in NAc shell by expressing a short hairpin RNA reduced cocaine reinforcement in similar tests, while overexpression of a dominant-negative CREB(S133A) mutant had no significant effect on cocaine self-administration. Cocaine 86-93 cAMP responsive element binding protein 1 Rattus norvegicus 26-30 22072694-7 2011 Finally, increasing CREB expression after withdrawal from self-administration enhanced cocaine-primed relapse, while reducing CREB levels facilitated extinction of cocaine seeking, but neither altered relapse induced by cocaine cues or footshock stress. Cocaine 87-94 cAMP responsive element binding protein 1 Rattus norvegicus 20-24 22072694-8 2011 Together, these findings indicate that CREB activity in NAc shell increases the motivation for cocaine during active self-administration or after withdrawal from cocaine. Cocaine 95-102 cAMP responsive element binding protein 1 Rattus norvegicus 39-43 22072694-8 2011 Together, these findings indicate that CREB activity in NAc shell increases the motivation for cocaine during active self-administration or after withdrawal from cocaine. Cocaine 162-169 cAMP responsive element binding protein 1 Rattus norvegicus 39-43 20451507-7 2010 These data suggest that the effects of CREB over expression on blunting cocaine reward could be, at least in part, attributed to the increased expression of the CART gene by direct interaction of P-CREB with the CART promoter CRE site, rather than by some indirect action. Cocaine 72-79 cAMP responsive element binding protein 1 Rattus norvegicus 39-43 21886557-2 2011 These changes are considered as consequences of cocaine-induced molecular adaptation such as CREB and c-Fos. Cocaine 48-55 cAMP responsive element binding protein 1 Rattus norvegicus 93-97 21886557-6 2011 In addition, LQ inhibited CREB phosphorylation and c-Fos expression in the striatum and the nucleus accumbens induced by acute cocaine. Cocaine 127-134 cAMP responsive element binding protein 1 Rattus norvegicus 26-30 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 cAMP responsive element binding protein 1 Rattus norvegicus 108-112 20613834-0 2010 Striatal microRNA controls cocaine intake through CREB signalling. Cocaine 27-34 cAMP responsive element binding protein 1 Rattus norvegicus 50-54 20613834-3 2010 Striatal miR-212 decreases responsiveness to the motivational properties of cocaine by markedly amplifying the stimulatory effects of the drug on cAMP response element binding protein (CREB) signalling. Cocaine 76-83 cAMP responsive element binding protein 1 Rattus norvegicus 146-183 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 cAMP responsive element binding protein 1 Rattus norvegicus 42-79 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 cAMP responsive element binding protein 1 Rattus norvegicus 81-85 21632938-6 2011 Our data are consistent with a cellular cascade whereby cocaine-induced activation of CREB promotes CREB-dependent transcription of NR2B and synaptic incorporation of NR2B-containing NMDARs, which generates new silent synapses within the NAc. Cocaine 56-63 cAMP responsive element binding protein 1 Rattus norvegicus 86-90 21632938-6 2011 Our data are consistent with a cellular cascade whereby cocaine-induced activation of CREB promotes CREB-dependent transcription of NR2B and synaptic incorporation of NR2B-containing NMDARs, which generates new silent synapses within the NAc. Cocaine 56-63 cAMP responsive element binding protein 1 Rattus norvegicus 100-104 21632938-7 2011 We propose that cocaine-induced activation of CREB and generation of new silent synapses may serve as key cellular events mediating cocaine-induced locomotor sensitization. Cocaine 16-23 cAMP responsive element binding protein 1 Rattus norvegicus 46-50 21632938-7 2011 We propose that cocaine-induced activation of CREB and generation of new silent synapses may serve as key cellular events mediating cocaine-induced locomotor sensitization. Cocaine 132-139 cAMP responsive element binding protein 1 Rattus norvegicus 46-50 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 cAMP responsive element binding protein 1 Rattus norvegicus 87-130 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 cAMP responsive element binding protein 1 Rattus norvegicus 132-136 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 184-191 cAMP responsive element binding protein 1 Rattus norvegicus 87-130 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 184-191 cAMP responsive element binding protein 1 Rattus norvegicus 132-136 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 cAMP responsive element binding protein 1 Rattus norvegicus 80-84 20613834-3 2010 Striatal miR-212 decreases responsiveness to the motivational properties of cocaine by markedly amplifying the stimulatory effects of the drug on cAMP response element binding protein (CREB) signalling. Cocaine 76-83 cAMP responsive element binding protein 1 Rattus norvegicus 185-189 20451507-7 2010 These data suggest that the effects of CREB over expression on blunting cocaine reward could be, at least in part, attributed to the increased expression of the CART gene by direct interaction of P-CREB with the CART promoter CRE site, rather than by some indirect action. Cocaine 72-79 cAMP responsive element binding protein 1 Rattus norvegicus 198-202 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 cAMP responsive element binding protein 1 Rattus norvegicus 44-48 19052730-0 2009 Sex differences in basal and cocaine-induced alterations in PKA and CREB proteins in the nucleus accumbens. Cocaine 29-36 cAMP responsive element binding protein 1 Rattus norvegicus 68-72 18598691-0 2008 Repeated cocaine administration increases N-methyl-d-aspartate NR1 subunit, extracellular signal-regulated kinase and cyclic AMP response element-binding protein phosphorylation and glutamate release in the rat dorsal striatum. Cocaine 9-16 cAMP responsive element binding protein 1 Rattus norvegicus 118-161 19046951-3 2009 Since over expression of CREB was shown to decrease cocaine-mediated reward, we hypothesized that CART could be a target gene for CREB in the NAc and that over expression of CREB would increase CART peptide levels. Cocaine 52-59 cAMP responsive element binding protein 1 Rattus norvegicus 25-29 19046951-3 2009 Since over expression of CREB was shown to decrease cocaine-mediated reward, we hypothesized that CART could be a target gene for CREB in the NAc and that over expression of CREB would increase CART peptide levels. Cocaine 52-59 cAMP responsive element binding protein 1 Rattus norvegicus 130-134 19046951-3 2009 Since over expression of CREB was shown to decrease cocaine-mediated reward, we hypothesized that CART could be a target gene for CREB in the NAc and that over expression of CREB would increase CART peptide levels. Cocaine 52-59 cAMP responsive element binding protein 1 Rattus norvegicus 130-134 18598691-7 2008 These findings suggest that glutamate release and dopamine D1 and NMDA receptor stimulation after repeated exposure to cocaine are associated with NMDA NR1 subunit, ERK1/2 and CREB phosphorylation in the dorsal striatum. Cocaine 119-126 cAMP responsive element binding protein 1 Rattus norvegicus 176-180 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 cAMP responsive element binding protein 1 Rattus norvegicus 104-141 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 cAMP responsive element binding protein 1 Rattus norvegicus 143-147 17324065-6 2007 The temporal and anatomical determinants of cocaine-induced CREB activity may indicate functional differences among NAc shell subregions and suggest the involvement of CREB in early and late cocaine effects. Cocaine 44-51 cAMP responsive element binding protein 1 Rattus norvegicus 168-172 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 cAMP responsive element binding protein 1 Rattus norvegicus 24-28 17324065-1 2007 The present study examined the differential cocaine-induced activation of the cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) throughout discrete zones of analysis of the nucleus accumbens (NAc) in rats. Cocaine 44-51 cAMP responsive element binding protein 1 Rattus norvegicus 150-154 17324065-2 2007 CREB-dependent gene transcription, which may underlie long-lasting drug-induced changes in behavior and the subjective effects of cocaine, varies depending on the stage of drug exposure or withdrawal and the cell population involved. Cocaine 130-137 cAMP responsive element binding protein 1 Rattus norvegicus 0-4 17324065-3 2007 Using immunohistochemistry, the authors analyzed changes in CREB phosphorylation in the NAc after 5 days of cocaine, a short or long drug-free period, and a subsequent challenge injection. Cocaine 108-115 cAMP responsive element binding protein 1 Rattus norvegicus 60-64 17324065-5 2007 Repeated cocaine resulted in CREB phosphorylation in all analyzed subregions of the NAc excluding the most ventrolateral region of the shell 2 weeks after cessation of repeated cocaine, but rats challenged after 2 drug-free days yielded a more localized activation of CREB in the 3 most dorsomedial zones of the shell. Cocaine 9-16 cAMP responsive element binding protein 1 Rattus norvegicus 29-33 17324065-5 2007 Repeated cocaine resulted in CREB phosphorylation in all analyzed subregions of the NAc excluding the most ventrolateral region of the shell 2 weeks after cessation of repeated cocaine, but rats challenged after 2 drug-free days yielded a more localized activation of CREB in the 3 most dorsomedial zones of the shell. Cocaine 9-16 cAMP responsive element binding protein 1 Rattus norvegicus 268-272 17324065-6 2007 The temporal and anatomical determinants of cocaine-induced CREB activity may indicate functional differences among NAc shell subregions and suggest the involvement of CREB in early and late cocaine effects. Cocaine 44-51 cAMP responsive element binding protein 1 Rattus norvegicus 60-64 17125745-0 2007 Alterations of CREB and DARPP-32 phosphorylation following cocaine and monoaminergic uptake inhibitors. Cocaine 59-66 cAMP responsive element binding protein 1 Rattus norvegicus 15-19 17125745-6 2007 A significant decrease in both phospho-CREB at Ser133 and phospho-DARPP-32 at Thr34 in the rat caudate putamen was produced by cocaine, GBR 12909, fluoxetine or nisoxetine. Cocaine 127-134 cAMP responsive element binding protein 1 Rattus norvegicus 39-43 15470197-1 2004 Prenatal exposure to cocaine has been shown to induce an increase in the myocardial expression and activation of the cAMP response binding protein (CREB), a transcriptional factor that has been shown to regulate gene expression. Cocaine 21-28 cAMP responsive element binding protein 1 Rattus norvegicus 117-146 16520736-3 2006 Decreasing excitability of NAc MSNs in vivo by overexpression of potassium channels enhanced locomotor responses to cocaine, suggesting that the increased NAc MSN excitability caused by CREB helped to limit behavioral sensitivity to cocaine. Cocaine 116-123 cAMP responsive element binding protein 1 Rattus norvegicus 186-190 16520736-3 2006 Decreasing excitability of NAc MSNs in vivo by overexpression of potassium channels enhanced locomotor responses to cocaine, suggesting that the increased NAc MSN excitability caused by CREB helped to limit behavioral sensitivity to cocaine. Cocaine 233-240 cAMP responsive element binding protein 1 Rattus norvegicus 186-190 16359811-0 2006 Antisense-induced reduction in nucleus accumbens cyclic AMP response element binding protein attenuates cocaine reinforcement. Cocaine 104-111 cAMP responsive element binding protein 1 Rattus norvegicus 49-92 16359811-1 2006 Repeated cocaine exposure up-regulates cyclic AMP signaling and increases the transcriptional activity of cyclic AMP response element binding protein (CREB) in the nucleus accumbens. Cocaine 9-16 cAMP responsive element binding protein 1 Rattus norvegicus 106-149 16359811-1 2006 Repeated cocaine exposure up-regulates cyclic AMP signaling and increases the transcriptional activity of cyclic AMP response element binding protein (CREB) in the nucleus accumbens. Cocaine 9-16 cAMP responsive element binding protein 1 Rattus norvegicus 151-155 16359811-4 2006 Similar infusions of CREB antisense in either core or shell produced a transient downward shift in cocaine self-administration dose-response curves on a fixed ratio 5 (five responses/injection) reinforcement schedule, indicating a reduction in cocaine reinforcement that fully recovered 3 days after treatment. Cocaine 99-106 cAMP responsive element binding protein 1 Rattus norvegicus 21-25 16359811-5 2006 CREB antisense also increased the threshold dose of cocaine required for reinstating cocaine self-administration, indicating that nucleus accumbens CREB levels regulate the incentive properties of cocaine. Cocaine 52-59 cAMP responsive element binding protein 1 Rattus norvegicus 0-4 16359811-5 2006 CREB antisense also increased the threshold dose of cocaine required for reinstating cocaine self-administration, indicating that nucleus accumbens CREB levels regulate the incentive properties of cocaine. Cocaine 52-59 cAMP responsive element binding protein 1 Rattus norvegicus 148-152 16359811-5 2006 CREB antisense also increased the threshold dose of cocaine required for reinstating cocaine self-administration, indicating that nucleus accumbens CREB levels regulate the incentive properties of cocaine. Cocaine 85-92 cAMP responsive element binding protein 1 Rattus norvegicus 0-4 16359811-5 2006 CREB antisense also increased the threshold dose of cocaine required for reinstating cocaine self-administration, indicating that nucleus accumbens CREB levels regulate the incentive properties of cocaine. Cocaine 85-92 cAMP responsive element binding protein 1 Rattus norvegicus 148-152 16359811-5 2006 CREB antisense also increased the threshold dose of cocaine required for reinstating cocaine self-administration, indicating that nucleus accumbens CREB levels regulate the incentive properties of cocaine. Cocaine 85-92 cAMP responsive element binding protein 1 Rattus norvegicus 0-4 16359811-5 2006 CREB antisense also increased the threshold dose of cocaine required for reinstating cocaine self-administration, indicating that nucleus accumbens CREB levels regulate the incentive properties of cocaine. Cocaine 85-92 cAMP responsive element binding protein 1 Rattus norvegicus 148-152 16359811-8 2006 These results suggest a necessary role for nucleus accumbens CREB activity in cocaine reinforcement, and, by converse analogy, up-regulation in CREB activity after chronic cocaine use could contribute to addiction-related increases in cocaine self-administration. Cocaine 78-85 cAMP responsive element binding protein 1 Rattus norvegicus 61-65 16359811-8 2006 These results suggest a necessary role for nucleus accumbens CREB activity in cocaine reinforcement, and, by converse analogy, up-regulation in CREB activity after chronic cocaine use could contribute to addiction-related increases in cocaine self-administration. Cocaine 172-179 cAMP responsive element binding protein 1 Rattus norvegicus 144-148 16219028-0 2005 Cocaine-induced CREB phosphorylation in nucleus accumbens of cocaine-sensitized rats is enabled by enhanced activation of extracellular signal-related kinase, but not protein kinase A. Cocaine 0-7 cAMP responsive element binding protein 1 Rattus norvegicus 16-20 16219028-0 2005 Cocaine-induced CREB phosphorylation in nucleus accumbens of cocaine-sensitized rats is enabled by enhanced activation of extracellular signal-related kinase, but not protein kinase A. Cocaine 61-68 cAMP responsive element binding protein 1 Rattus norvegicus 16-20 16219028-2 2005 We hypothesized that the same treatment regimen would also enhance cocaine-induced activation of intracellular signaling kinases that phosphorylate cyclic AMP-regulated element-binding protein (CREB), an important mediator of c-fos transcription. Cocaine 67-74 cAMP responsive element binding protein 1 Rattus norvegicus 148-192 16219028-2 2005 We hypothesized that the same treatment regimen would also enhance cocaine-induced activation of intracellular signaling kinases that phosphorylate cyclic AMP-regulated element-binding protein (CREB), an important mediator of c-fos transcription. Cocaine 67-74 cAMP responsive element binding protein 1 Rattus norvegicus 194-198 16219028-5 2005 Using western blots and immunohistochemistry, we detected cocaine-induced CREB phosphorylation after repeated cocaine administration, but not after repeated saline administration. Cocaine 58-65 cAMP responsive element binding protein 1 Rattus norvegicus 74-78 16219028-5 2005 Using western blots and immunohistochemistry, we detected cocaine-induced CREB phosphorylation after repeated cocaine administration, but not after repeated saline administration. Cocaine 110-117 cAMP responsive element binding protein 1 Rattus norvegicus 74-78 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 cAMP responsive element binding protein 1 Rattus norvegicus 114-118 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 cAMP responsive element binding protein 1 Rattus norvegicus 89-93 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 cAMP responsive element binding protein 1 Rattus norvegicus 89-93 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 cAMP responsive element binding protein 1 Rattus norvegicus 172-176 15470197-1 2004 Prenatal exposure to cocaine has been shown to induce an increase in the myocardial expression and activation of the cAMP response binding protein (CREB), a transcriptional factor that has been shown to regulate gene expression. Cocaine 21-28 cAMP responsive element binding protein 1 Rattus norvegicus 148-152 11549750-0 2001 Altered responsiveness to cocaine and increased immobility in the forced swim test associated with elevated cAMP response element-binding protein expression in nucleus accumbens. Cocaine 26-33 cAMP responsive element binding protein 1 Rattus norvegicus 108-145 12595601-3 2003 Because CREB expression and activation in specific brain regions are modified after chronic cocaine administration, we sought to determine whether chronic perinatal cocaine exposure affects the expression of CREB and p-CREB in the postnatal rat heart. Cocaine 165-172 cAMP responsive element binding protein 1 Rattus norvegicus 208-212 12595601-3 2003 Because CREB expression and activation in specific brain regions are modified after chronic cocaine administration, we sought to determine whether chronic perinatal cocaine exposure affects the expression of CREB and p-CREB in the postnatal rat heart. Cocaine 165-172 cAMP responsive element binding protein 1 Rattus norvegicus 208-212 12595601-9 2003 Our results suggest that perinatal cocaine exposure stimulates CREB activation in the neonatal heart, and it may be mediated by different mechanisms at d 1 and d 7. Cocaine 35-42 cAMP responsive element binding protein 1 Rattus norvegicus 63-67 11739600-4 2001 Antisense technology was used to produce a local knockdown of CREB in the lateral caudate-putamen, a region that mediates the dyskinetic or stereotypic manifestations associated with l-DOPA or cocaine treatment, respectively. Cocaine 193-200 cAMP responsive element binding protein 1 Rattus norvegicus 62-66 11739600-5 2001 In intact rats, CREB antisense reduced both basal and cocaine-induced expression of c-Fos, FosB/DeltaFosB, and prodynorphin mRNA. Cocaine 54-61 cAMP responsive element binding protein 1 Rattus norvegicus 16-20 14727002-1 2004 RATIONALE: Elevations in cAMP response element binding protein (CREB) function within the mesolimbic system of rats reduce cocaine reward in place conditioning studies and increase immobility in the forced swim test. Cocaine 123-130 cAMP responsive element binding protein 1 Rattus norvegicus 25-62 14727002-1 2004 RATIONALE: Elevations in cAMP response element binding protein (CREB) function within the mesolimbic system of rats reduce cocaine reward in place conditioning studies and increase immobility in the forced swim test. Cocaine 123-130 cAMP responsive element binding protein 1 Rattus norvegicus 64-68 12595601-0 2003 Perinatal cocaine exposure stimulates the expression and activation of CREB in the neonatal rat heart. Cocaine 10-17 cAMP responsive element binding protein 1 Rattus norvegicus 71-75 11549750-4 2001 Conversely, rats treated with HSV-CREB spent less time in cocaine-associated environments, indicating increased cocaine aversion. Cocaine 58-65 cAMP responsive element binding protein 1 Rattus norvegicus 34-38 11549750-5 2001 Studies in which drug-environment pairings were varied to coincide with either the early or late effects of cocaine suggest that CREB-associated place aversions reflect increased cocaine withdrawal. Cocaine 108-115 cAMP responsive element binding protein 1 Rattus norvegicus 129-133 9856954-2 1998 Overexpression of CREB in this region decreases the rewarding effects of cocaine and makes low doses of the drug aversive. Cocaine 73-80 cAMP responsive element binding protein 1 Rattus norvegicus 18-22 9856954-3 1998 Conversely, overexpression of a dominant-negative mutant CREB increases the rewarding effects of cocaine. Cocaine 97-104 cAMP responsive element binding protein 1 Rattus norvegicus 57-61 9856954-5 1998 Moreover, blockade of kappa opioid receptors (on which dynorphin acts) antagonizes the negative effect of CREB on cocaine reward. Cocaine 114-121 cAMP responsive element binding protein 1 Rattus norvegicus 106-110 8385579-9 1993 The investigations have focused on the Fos-Jun family of immediate early gene transcription factors, and the CREB family of transcription factors, as possible mediators of the effects of chronic opiate and cocaine exposure on regulation of neuronal gene expression. Cocaine 206-213 cAMP responsive element binding protein 1 Rattus norvegicus 109-113