PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30150424-7 2018 Overexpression of CREB or knockdown of p66shc restored simvastatin-dependent induction of HO1 and MnSOD in the presence of nicotine. Nicotine 123-131 cAMP responsive element binding protein 1 Rattus norvegicus 18-22 32417176-0 2020 Expression analysis of hippocampal and amygdala CREB-BDNF signaling pathway in nicotine-induced reward under stress in rats. Nicotine 79-87 cAMP responsive element binding protein 1 Rattus norvegicus 48-52 32417176-2 2020 The present study includes an expression analysis to identify the possible role of hippocampal and amygdala CREB (cAMP response element-binding protein) and BDNF (Brain-derived neurotrophic factor) activation in nicotine-induced conditioned place preference (CPP) under exposure to acute or sub-chronic stress. Nicotine 212-220 cAMP responsive element binding protein 1 Rattus norvegicus 108-112 32417176-2 2020 The present study includes an expression analysis to identify the possible role of hippocampal and amygdala CREB (cAMP response element-binding protein) and BDNF (Brain-derived neurotrophic factor) activation in nicotine-induced conditioned place preference (CPP) under exposure to acute or sub-chronic stress. Nicotine 212-220 cAMP responsive element binding protein 1 Rattus norvegicus 114-151 32417176-3 2020 Using western-blot technique, CREB phosphorylation was shown to increase in the hippocampus and the amygdala following nicotine-induced CPP. Nicotine 119-127 cAMP responsive element binding protein 1 Rattus norvegicus 30-34 32417176-5 2020 In animals exposed to acute stress, the amygdala ratios of the pCREB/CREB decreased, while pre-treatment of the animals with nicotine (0.1 mg/kg) decreased this ratio only in the hippocampus. Nicotine 125-133 cAMP responsive element binding protein 1 Rattus norvegicus 64-68 32417176-7 2020 Interestingly, sub-chronic stress-induced increase of nicotine reward only decreased the hippocampal pCREB/CREB ratio. Nicotine 54-62 cAMP responsive element binding protein 1 Rattus norvegicus 102-106 32417176-11 2020 In summary, the present study indicate that the alterations of the ratio of pCREB/CREB and also the level of BDNF in the hippocampus may be critical for enhancing nicotine reward under stress condition. Nicotine 163-171 cAMP responsive element binding protein 1 Rattus norvegicus 77-81 32174265-7 2020 Immunoblotting revealed a >2-fold increase in phosphorylation of CREB with nicotine, peaking at 4 h. Nicotine treatment of cells increased viability from 35% to 54%, and Bcl-2 immunoreactivity increased by 1.4-fold. Nicotine 75-83 cAMP responsive element binding protein 1 Rattus norvegicus 65-69 32174265-7 2020 Immunoblotting revealed a >2-fold increase in phosphorylation of CREB with nicotine, peaking at 4 h. Nicotine treatment of cells increased viability from 35% to 54%, and Bcl-2 immunoreactivity increased by 1.4-fold. Nicotine 101-109 cAMP responsive element binding protein 1 Rattus norvegicus 65-69 31047996-0 2019 Nitric oxide blockade in mediodorsal thalamus impaired nicotine/ethanol-induced memory retrieval in rats via inhibition of prefrontal cortical pCREB/CREB signaling pathway. Nicotine 55-63 cAMP responsive element binding protein 1 Rattus norvegicus 144-148 31047996-12 2019 Ethanol-induced amnesia, however, decreased this ratio in the PFC while the co-administration of nicotine and ethanol increased the PFC CREB signaling. Nicotine 97-105 cAMP responsive element binding protein 1 Rattus norvegicus 136-140 31047996-13 2019 Interestingly, the inhibitory effect of L-NAME and the potentiating effect of l-arginine on nicotine response were associated with the decrease and increase of the PFC p-CREB/CREB ratio respectively. Nicotine 92-100 cAMP responsive element binding protein 1 Rattus norvegicus 170-174 31047996-13 2019 Interestingly, the inhibitory effect of L-NAME and the potentiating effect of l-arginine on nicotine response were associated with the decrease and increase of the PFC p-CREB/CREB ratio respectively. Nicotine 92-100 cAMP responsive element binding protein 1 Rattus norvegicus 175-179 30150424-1 2018 BACKGROUND/AIM: We have previously reported that simvastatin exhibits antioxidant properties via extracellular signal-regulated kinase (ERK)/cAMP-response element binding (CREB) protein-dependent induction of heme oxygenase-1 (HO1) and chronic nicotine exposure inhibits ERK/CREB signaling in renal proximal tubule cells (through p66shc). Nicotine 244-252 cAMP responsive element binding protein 1 Rattus norvegicus 172-176 30150424-6 2018 RESULTS: Nicotine suppressed simvastatin-dependent activation of HO1 and MnSOD promoters and activity of CREB and ELK1 via p66shc. Nicotine 9-17 cAMP responsive element binding protein 1 Rattus norvegicus 105-109 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. Nicotine 240-248 cAMP responsive element binding protein 1 Rattus norvegicus 56-93 28608236-0 2017 The Neuroprotective Effect of Curcumin Against Nicotine-Induced Neurotoxicity is Mediated by CREB-BDNF Signaling Pathway. Nicotine 47-55 cAMP responsive element binding protein 1 Rattus norvegicus 93-97 28608236-3 2017 The current study was designed to evaluate the role of CREB-BDNF signaling in mediating the neuroprotective effects of curcumin against nicotine-induced apoptosis, oxidative stress and inflammation in rats. Nicotine 136-144 cAMP responsive element binding protein 1 Rattus norvegicus 55-59 28608236-12 2017 In addition, nicotine treatment increased lipid peroxidation and the levels of GSH, IL-1beta, TNF-alpha and Bax, while reducing Bcl-2, P-CREB and BDNF levels in the hippocampus. Nicotine 13-21 cAMP responsive element binding protein 1 Rattus norvegicus 137-141 28608236-15 2017 Thus, curcumin via activation of P-CREB/BDNF signaling pathway, confers neuroprotection against nicotine-induced inflammation, apoptosis and oxidative stress. Nicotine 96-104 cAMP responsive element binding protein 1 Rattus norvegicus 35-39 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. Nicotine 240-248 cAMP responsive element binding protein 1 Rattus norvegicus 95-99 24277525-0 2014 Chronic nicotine treatment reverses hypothyroidism-induced impairment of L-LTP induction phase: critical role of CREB. Nicotine 8-16 cAMP responsive element binding protein 1 Rattus norvegicus 113-117 25981209-11 2015 Expression of nicotine-induced CPP was accompanied by an increase of phospho-CREB (cyclic AMP-responsive element-binding protein) and HDAC2 (histone deacetylase 2) expression in the nucleus accumbens. Nicotine 14-22 cAMP responsive element binding protein 1 Rattus norvegicus 77-81 24277525-6 2014 Five minutes after MHFS, Western blotting showed an increase in the levels of P-CREB, and P-MAPKp42/44 in sham-operated control, nicotine, and nicotine-treated hypothyroid animals, but not in hypothyroid animals. Nicotine 143-151 cAMP responsive element binding protein 1 Rattus norvegicus 80-84 24277525-8 2014 Therefore, normalized phosphorylation of essential kinases such as P-CREB and P-MAPK p42/44 in the CA1 area of nicotine-treated hypothyroid animals plays a crucial role in nicotine-induced rescue of L-LTP induction during hypothyroidism. Nicotine 111-119 cAMP responsive element binding protein 1 Rattus norvegicus 69-73 24277525-8 2014 Therefore, normalized phosphorylation of essential kinases such as P-CREB and P-MAPK p42/44 in the CA1 area of nicotine-treated hypothyroid animals plays a crucial role in nicotine-induced rescue of L-LTP induction during hypothyroidism. Nicotine 172-180 cAMP responsive element binding protein 1 Rattus norvegicus 69-73 21740234-0 2012 Chronic nicotine administration impairs activation of cyclic AMP-response element binding protein and survival of newborn cells in the dentate gyrus. Nicotine 8-16 cAMP responsive element binding protein 1 Rattus norvegicus 54-97 21740234-2 2012 Here, we demonstrate that chronic nicotine administration in adult rats inactivates the cyclic AMP-response element binding protein (CREB), a transcription factor that regulates neurogenesis and other plasticity-related processes necessary for learning and memory. Nicotine 34-42 cAMP responsive element binding protein 1 Rattus norvegicus 88-131 21740234-2 2012 Here, we demonstrate that chronic nicotine administration in adult rats inactivates the cyclic AMP-response element binding protein (CREB), a transcription factor that regulates neurogenesis and other plasticity-related processes necessary for learning and memory. Nicotine 34-42 cAMP responsive element binding protein 1 Rattus norvegicus 133-137 21740234-5 2012 Additionally, we found that retroviral-mediated expression of a constitutively active CREB in the dentate gyrus rescues survival of newborn cells and reverses the nicotine-induced decline in the number of mature granule neurons. Nicotine 163-171 cAMP responsive element binding protein 1 Rattus norvegicus 86-90 21740234-6 2012 Prolonged nicotine exposure also compromises CREB activation and reduces the viability of progenitor cells in vitro, thereby suggesting that nicotine may exert its adverse effects directly on immature cells in vivo. Nicotine 10-18 cAMP responsive element binding protein 1 Rattus norvegicus 45-49 21740234-7 2012 Taken together, these data demonstrate that inhibition of CREB activation is responsible for the nicotine-induced impairment of hippocampal plasticity. Nicotine 97-105 cAMP responsive element binding protein 1 Rattus norvegicus 58-62 17523180-3 2007 Immunoblots analysis showed that chronic nicotine treatment of hypothyroid rats prevented the reduction in the basal protein levels of adenylyl cyclase I (ACI), mitogen-activated protein kinases [MAPKp44/42 (ERK1/2)], calcium-calmodulin-dependent protein kinase IV (CaMKIV), and cyclic-AMP response element binding protein [CREB; phosphorylated (P-) and total]. Nicotine 41-49 cAMP responsive element binding protein 1 Rattus norvegicus 279-322 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. Nicotine 222-230 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. Nicotine 222-230 cAMP responsive element binding protein 1 Rattus norvegicus 81-85 21420997-6 2011 In the nicotine-treated groups, the levels of phosphorylated CREB and ERK2 in the PFC were increased in HIV-1Tg rats, but decreased in F344 animals. Nicotine 7-15 cAMP responsive element binding protein 1 Rattus norvegicus 61-65 21420997-8 2011 These results demonstrate that HIV-1 viral proteins produce differences in basal and nicotine-induced alterations in CREB and ERK signaling that may contribute to the alteration in psychomotor sensitization. Nicotine 85-93 cAMP responsive element binding protein 1 Rattus norvegicus 117-121 21420997-9 2011 Thus, HIV-1 positive smokers are possibly more vulnerable to alterations in CREB and ERK signaling and this has implications for motivated behavior, including tobacco smoking, in HIV-1 positive individuals who self-administer nicotine. Nicotine 226-234 cAMP responsive element binding protein 1 Rattus norvegicus 76-80 20047710-2 2010 Nicotinic acetylcholine receptors (nAChRs) are involved in nicotine-induced phosphorylation of CREB (cyclic AMP response element-binding protein) in PC12h cells. Nicotine 59-67 cAMP responsive element binding protein 1 Rattus norvegicus 95-99 20047710-2 2010 Nicotinic acetylcholine receptors (nAChRs) are involved in nicotine-induced phosphorylation of CREB (cyclic AMP response element-binding protein) in PC12h cells. Nicotine 59-67 cAMP responsive element binding protein 1 Rattus norvegicus 101-144 19711055-0 2009 Nicotine-conditioned place preference induced CREB phosphorylation and Fos expression in the adult rat brain. Nicotine 0-8 cAMP responsive element binding protein 1 Rattus norvegicus 46-50 19711055-9 2009 CONCLUSION: The results indicate that the phosphorylation of CREB and expression of Fos protein, as indicators of neural activity, accompany the acquisition and maintenance of nicotine-induced CPP but not CPA in mesolimbic areas (NAc, VTA, PFC, and DStr) as well as in memory consolidation structures (hippocampus and amygdala) and nicotinic receptor are involved in this process. Nicotine 176-184 cAMP responsive element binding protein 1 Rattus norvegicus 61-65 22952905-0 2012 Environmental enrichment alters nicotine-mediated locomotor sensitization and phosphorylation of DARPP-32 and CREB in rat prefrontal cortex. Nicotine 32-40 cAMP responsive element binding protein 1 Rattus norvegicus 110-114 22952905-6 2012 Moreover, EC rats had lower basal phosphorylation levels of CREB at serine 133 in PFC and nucleus accumbens compared to IC and SC rats, whereas the nicotine-induced increase in phosphorylated CREB-Ser133 was more pronounced in PFC of EC rats relative to IC and SC rats. Nicotine 148-156 cAMP responsive element binding protein 1 Rattus norvegicus 60-64 22952905-6 2012 Moreover, EC rats had lower basal phosphorylation levels of CREB at serine 133 in PFC and nucleus accumbens compared to IC and SC rats, whereas the nicotine-induced increase in phosphorylated CREB-Ser133 was more pronounced in PFC of EC rats relative to IC and SC rats. Nicotine 148-156 cAMP responsive element binding protein 1 Rattus norvegicus 192-196 17523180-3 2007 Immunoblots analysis showed that chronic nicotine treatment of hypothyroid rats prevented the reduction in the basal protein levels of adenylyl cyclase I (ACI), mitogen-activated protein kinases [MAPKp44/42 (ERK1/2)], calcium-calmodulin-dependent protein kinase IV (CaMKIV), and cyclic-AMP response element binding protein [CREB; phosphorylated (P-) and total]. Nicotine 41-49 cAMP responsive element binding protein 1 Rattus norvegicus 324-328 17523180-4 2007 A significant increase in the levels of P-CREB, P-MAPKp44, P-MAPKp42 and brain derived neurotrophic factor (BDNF) was seen 4 h after multiple train high frequency stimulation (MHFS) in nicotine-treated hypothyroid and control animals, but not in hypothyroid animals. Nicotine 185-193 cAMP responsive element binding protein 1 Rattus norvegicus 42-46 17523180-6 2007 These findings suggest that prevention of the reduced basal level of CaMKIV, MAPKp44/42, and CREB by nicotine along with the regained ability of MHFS to induce MAPKp44/42 and CREB phosphorylation in nicotine treated hypothyroid animals may be responsible for the reversal of L-LTP impairment by chronic nicotine treatment in this disease model. Nicotine 101-109 cAMP responsive element binding protein 1 Rattus norvegicus 93-97 16452470-3 2006 Treatment of PC12 cells with 200 microm nicotine triggered rapid but transient elevation of P-CREB followed by a second sustained rise after 2-5 h of continuous nicotine. Nicotine 40-48 cAMP responsive element binding protein 1 Rattus norvegicus 94-98 16452470-0 2006 Prolonged activation of cAMP-response element-binding protein and ATF-2 needed for nicotine-triggered elevation of tyrosine hydroxylase gene transcription in PC12 cells. Nicotine 83-91 cAMP responsive element binding protein 1 Rattus norvegicus 24-61 16452470-1 2006 Phosphorylation (P-) of cAMP-response element-binding protein (CREB) by protein kinase A or mitogen-activated protein kinases was implicated in mediating the increased tyrosine hydroxylase (TH) gene expression after prolonged exposure to nicotine in vivo and in cell culture. Nicotine 238-246 cAMP responsive element binding protein 1 Rattus norvegicus 24-61 16452470-1 2006 Phosphorylation (P-) of cAMP-response element-binding protein (CREB) by protein kinase A or mitogen-activated protein kinases was implicated in mediating the increased tyrosine hydroxylase (TH) gene expression after prolonged exposure to nicotine in vivo and in cell culture. Nicotine 238-246 cAMP responsive element binding protein 1 Rattus norvegicus 63-67 16631827-0 2006 L-type calcium channel ligands block nicotine-induced signaling to CREB by inhibiting nicotinic receptors. Nicotine 37-45 cAMP responsive element binding protein 1 Rattus norvegicus 67-71 16631827-4 2006 We found that 10microM nicotine and 40mM K(+) both reversibly depolarize SCG neurons to -20mV, sufficient to activate LTCCs and downstream signaling, including induction of nuclear phospho-CREB (pCREB); this induction was blocked by LTCC antagonists. Nicotine 23-31 cAMP responsive element binding protein 1 Rattus norvegicus 189-193 16631827-5 2006 Interestingly, the effects of LTCC antagonists on nicotine-induced signaling to CREB are not mediated by their actions on LTCCs, but rather via inhibition of nAChRs, which prevents nicotine-induced depolarization. Nicotine 50-58 cAMP responsive element binding protein 1 Rattus norvegicus 80-84 16631827-5 2006 Interestingly, the effects of LTCC antagonists on nicotine-induced signaling to CREB are not mediated by their actions on LTCCs, but rather via inhibition of nAChRs, which prevents nicotine-induced depolarization. Nicotine 181-189 cAMP responsive element binding protein 1 Rattus norvegicus 80-84 16452470-6 2006 In contrast, protein kinase A inhibitor H-89 or Ca(2+)/calmodulin-activated protein kinase inhibitor KN-93 reduced the nicotine-triggered rise in P-CREB and TH promoter activity. Nicotine 119-127 cAMP responsive element binding protein 1 Rattus norvegicus 148-152 16452470-11 2006 Knockdown of ATF-2 or CREB with siRNA did not alter basal TH promoter activity or mRNA but greatly attenuated the response to nicotine. Nicotine 126-134 cAMP responsive element binding protein 1 Rattus norvegicus 22-26 16452470-12 2006 The results suggest that both ATF-2 and CREB mediate activation of TH gene transcription by nicotine. Nicotine 92-100 cAMP responsive element binding protein 1 Rattus norvegicus 40-44 15935216-6 2005 The chronic nicotine treatment also resulted, after 2 days of continuous administration in significant activation of the transcription factor CREB and the ERK/MAPK survival kinase in the Hb, suggesting that these alterations in expression are in some way related to the neurodegenerative/neuroreparative process. Nicotine 12-20 cAMP responsive element binding protein 1 Rattus norvegicus 142-146 15334606-0 2004 Modulation of CREB expression and phosphorylation in the rat nucleus accumbens during nicotine exposure and withdrawal. Nicotine 86-94 cAMP responsive element binding protein 1 Rattus norvegicus 14-18 15334606-2 2004 To understand the molecular mechanisms of nicotine addiction, the present investigation examined the effects of acute and chronic nicotine treatment and its withdrawal on cAMP-responsive element binding (CREB) protein expression and phosphorylation (serine-133) in nucleus accumbens (NAc) structures of rats. Nicotine 130-138 cAMP responsive element binding protein 1 Rattus norvegicus 171-202 15334606-2 2004 To understand the molecular mechanisms of nicotine addiction, the present investigation examined the effects of acute and chronic nicotine treatment and its withdrawal on cAMP-responsive element binding (CREB) protein expression and phosphorylation (serine-133) in nucleus accumbens (NAc) structures of rats. Nicotine 130-138 cAMP responsive element binding protein 1 Rattus norvegicus 204-208 15334606-4 2004 On the other hand, 18-hr withdrawal after chronic nicotine exposure produced significant reductions in the total CREB and p-CREB protein levels in the shell but not in core structures of nac. Nicotine 50-58 cAMP responsive element binding protein 1 Rattus norvegicus 113-117 15334606-4 2004 On the other hand, 18-hr withdrawal after chronic nicotine exposure produced significant reductions in the total CREB and p-CREB protein levels in the shell but not in core structures of nac. Nicotine 50-58 cAMP responsive element binding protein 1 Rattus norvegicus 124-128 15334606-5 2004 interestingly, nicotine withdrawal (1 hr) after chronic exposure maintained normal levels of total CREB and p-CREB protein levels in the shell and core structures of NAc. Nicotine 15-23 cAMP responsive element binding protein 1 Rattus norvegicus 99-103 15334606-5 2004 interestingly, nicotine withdrawal (1 hr) after chronic exposure maintained normal levels of total CREB and p-CREB protein levels in the shell and core structures of NAc. Nicotine 15-23 cAMP responsive element binding protein 1 Rattus norvegicus 110-114 15334606-6 2004 These results suggest the possibility that decreased CREB activity in the shell of NAc may be associated with abnormal reward mechanisms during nicotine withdrawal after chronic exposure. Nicotine 144-152 cAMP responsive element binding protein 1 Rattus norvegicus 53-57 15164609-8 2004 Nicotine induces the activation of both PI3 kinase/Act and ERK/CREB pathways via common pathways including non-alpha 7-nAChRs, L-type VSCC, CaM kinase and EGFR in PC12h cells, but Src family tyrosine kinases only participate in the pathway to activate Akt. Nicotine 0-8 cAMP responsive element binding protein 1 Rattus norvegicus 63-67 12504594-3 2002 We show here that nicotine can alter gene expression in rat hippocampal neurons, as reflected by activation of the transcription factor CREB and appearance of the immediate early gene product c-Fos. Nicotine 18-26 cAMP responsive element binding protein 1 Rattus norvegicus 136-140 11701752-0 2001 Nicotine-induced phosphorylation of extracellular signal-regulated protein kinase and CREB in PC12h cells. Nicotine 0-8 cAMP responsive element binding protein 1 Rattus norvegicus 86-90 11701752-1 2001 We have investigated mechanisms of nicotine-induced phosphorylation of extracellular signal-regulated protein kinase (p42/44 MAP kinase, ERK) and cAMP response element binding protein (CREB) in PC12h cells. Nicotine 35-43 cAMP responsive element binding protein 1 Rattus norvegicus 146-183 11701752-1 2001 We have investigated mechanisms of nicotine-induced phosphorylation of extracellular signal-regulated protein kinase (p42/44 MAP kinase, ERK) and cAMP response element binding protein (CREB) in PC12h cells. Nicotine 35-43 cAMP responsive element binding protein 1 Rattus norvegicus 185-189 11701752-8 2001 A calmodulin antagonist, a CaM kinase inhibitor, a MAP kinase kinase inhibitor inhibited nicotine-induced ERK and CREB phosphorylation. Nicotine 89-97 cAMP responsive element binding protein 1 Rattus norvegicus 114-118 11701752-9 2001 The time course of the phosphorylation of CREB induced by nicotine was similar to that of ERK induced by nicotine. Nicotine 58-66 cAMP responsive element binding protein 1 Rattus norvegicus 42-46 11701752-10 2001 These results suggest that non-alpha7 nAChRs are involved in nicotine-induced ERK phosphorylation through CaM kinase and the Ras-MAP kinase cascade and most of the nicotine-induced CREB phosphorylation is mediated by the ERK phosphorylation in PC12h cells. Nicotine 61-69 cAMP responsive element binding protein 1 Rattus norvegicus 181-185 11701752-10 2001 These results suggest that non-alpha7 nAChRs are involved in nicotine-induced ERK phosphorylation through CaM kinase and the Ras-MAP kinase cascade and most of the nicotine-induced CREB phosphorylation is mediated by the ERK phosphorylation in PC12h cells. Nicotine 164-172 cAMP responsive element binding protein 1 Rattus norvegicus 181-185 9658190-10 1998 Expression of the CREB antagonist KCREB blocked the response of the chromogranin A promoter to nicotine, cAMP, or MAPK pathway activation by either chemical stimulation or cotransfection of active cascade components. Nicotine 95-103 cAMP responsive element binding protein 1 Rattus norvegicus 18-22 7494448-6 1995 Nicotine administration by injection increased the phosphorylation of CREB and induced c-Fos protein without affecting members of the jun family. Nicotine 0-8 cAMP responsive element binding protein 1 Rattus norvegicus 70-74 15164609-7 2004 Nicotine transiently activates phosphorylation of ERK-, CREB and Akt. Nicotine 0-8 cAMP responsive element binding protein 1 Rattus norvegicus 56-60 12269402-5 2002 The repeated nicotine administrations also elevated phospho-CREB without altering total CREB level in all tested groups. Nicotine 13-21 cAMP responsive element binding protein 1 Rattus norvegicus 60-64 11331423-0 2001 Effects of protracted nicotine exposure and withdrawal on the expression and phosphorylation of the CREB gene transcription factor in rat brain. Nicotine 22-30 cAMP responsive element binding protein 1 Rattus norvegicus 100-104 11331423-1 2001 Addiction to nicotine may result in molecular adaptations in the neurocircuitry of specific brain structures via changes in the cyclic AMP-responsive element binding protein (CREB)-dependent gene transcription program. Nicotine 13-21 cAMP responsive element binding protein 1 Rattus norvegicus 128-173 11331423-1 2001 Addiction to nicotine may result in molecular adaptations in the neurocircuitry of specific brain structures via changes in the cyclic AMP-responsive element binding protein (CREB)-dependent gene transcription program. Nicotine 13-21 cAMP responsive element binding protein 1 Rattus norvegicus 175-179 11331423-4 2001 On the other hand, decreases in the expression of CREB protein and phosphorylation of CREB occur in the cingulate gyrus, and in the parietal and the piriform but not in the frontal cortex during nicotine withdrawal (18 h) after nicotine exposure. Nicotine 195-203 cAMP responsive element binding protein 1 Rattus norvegicus 50-54 11331423-4 2001 On the other hand, decreases in the expression of CREB protein and phosphorylation of CREB occur in the cingulate gyrus, and in the parietal and the piriform but not in the frontal cortex during nicotine withdrawal (18 h) after nicotine exposure. Nicotine 195-203 cAMP responsive element binding protein 1 Rattus norvegicus 86-90 11331423-4 2001 On the other hand, decreases in the expression of CREB protein and phosphorylation of CREB occur in the cingulate gyrus, and in the parietal and the piriform but not in the frontal cortex during nicotine withdrawal (18 h) after nicotine exposure. Nicotine 228-236 cAMP responsive element binding protein 1 Rattus norvegicus 50-54 11331423-4 2001 On the other hand, decreases in the expression of CREB protein and phosphorylation of CREB occur in the cingulate gyrus, and in the parietal and the piriform but not in the frontal cortex during nicotine withdrawal (18 h) after nicotine exposure. Nicotine 228-236 cAMP responsive element binding protein 1 Rattus norvegicus 86-90 11331423-5 2001 It was also observed that CREB and p-CREB protein levels were significantly decreased in the medial and basolateral, but not in the central amygdala during nicotine withdrawal (18 h) after chronic nicotine exposure. Nicotine 156-164 cAMP responsive element binding protein 1 Rattus norvegicus 26-30 11331423-5 2001 It was also observed that CREB and p-CREB protein levels were significantly decreased in the medial and basolateral, but not in the central amygdala during nicotine withdrawal (18 h) after chronic nicotine exposure. Nicotine 156-164 cAMP responsive element binding protein 1 Rattus norvegicus 37-41 11331423-5 2001 It was also observed that CREB and p-CREB protein levels were significantly decreased in the medial and basolateral, but not in the central amygdala during nicotine withdrawal (18 h) after chronic nicotine exposure. Nicotine 197-205 cAMP responsive element binding protein 1 Rattus norvegicus 26-30 11331423-5 2001 It was also observed that CREB and p-CREB protein levels were significantly decreased in the medial and basolateral, but not in the central amygdala during nicotine withdrawal (18 h) after chronic nicotine exposure. Nicotine 197-205 cAMP responsive element binding protein 1 Rattus norvegicus 37-41 11331423-8 2001 These results provide the first evidence that decreased CREB activity and/or expression in specific cortical and amygdaloid brain structures may be involved in the underlying molecular mechanisms of nicotine dependence. Nicotine 199-207 cAMP responsive element binding protein 1 Rattus norvegicus 56-60