PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 32028757-10 2020 In addition, structural changes caused by stress and blocking the changes by imipramine were corelated well with altered activation and expression of synaptic plasticity-promoting molecules such as phospho-CREB, phospho-CAMKII, and PSD-95. Imipramine 77-87 cAMP responsive element binding protein 1 Mus musculus 206-210 20122921-2 2010 Recently, chronic psychosocial stress as animal model of depression has been shown to stimulate CREB transcriptional activity in the brain; this stimulation was prevented by treatment with the antidepressant imipramine, which inhibits both noradrenaline and serotonin reuptake. Imipramine 208-218 cAMP responsive element binding protein 1 Mus musculus 96-100 24036107-7 2014 Co-administration of 9h of fasting and imipramine (30mg/kg, i.p) produced the additive antidepressant-like effects in the FST and increased the ratio of p-CREB/CREB. Imipramine 39-49 cAMP responsive element binding protein 1 Mus musculus 155-159 24036107-7 2014 Co-administration of 9h of fasting and imipramine (30mg/kg, i.p) produced the additive antidepressant-like effects in the FST and increased the ratio of p-CREB/CREB. Imipramine 39-49 cAMP responsive element binding protein 1 Mus musculus 160-164 26481532-4 2015 OBJECTIVE AND METHODS: In the present study we investigated whether acute or chronic treatment with imipramine, escitalopram, reboxetine and bupropion would cause changes in CREB, BDNF, TrkB and GPR39-Zn(2+) receptor proteins (measured by Western Blot) in the frontal cortex of mice fed with a low-zinc diet. Imipramine 100-110 cAMP responsive element binding protein 1 Mus musculus 174-178 23816950-1 2013 UNLABELLED: The effect of long-term administration of imipramine, a tricyclic antidepressant, on the phosphorylation status of cyclic adenosine monophosphate-responsive element-binding protein (CREB), mitogen-activated protein kinase family members, and phospholipase gamma-1 (PLCgamma-1) was investigated in the dorsal horn of the spinal cord following peripheral nerve lesion. Imipramine 54-64 cAMP responsive element binding protein 1 Mus musculus 127-192 23816950-1 2013 UNLABELLED: The effect of long-term administration of imipramine, a tricyclic antidepressant, on the phosphorylation status of cyclic adenosine monophosphate-responsive element-binding protein (CREB), mitogen-activated protein kinase family members, and phospholipase gamma-1 (PLCgamma-1) was investigated in the dorsal horn of the spinal cord following peripheral nerve lesion. Imipramine 54-64 cAMP responsive element binding protein 1 Mus musculus 194-198 23816950-6 2013 Moreover, imipramine therapy reversed nerve injury-induced CREB and PLCgamma-1 phosphorylation but had no effect on ERK1,2, p38, and c-Jun N-terminal kinase activity. Imipramine 10-20 cAMP responsive element binding protein 1 Mus musculus 59-63 23816950-9 2013 Our data also provide evidence that prolonged imipramine treatment may induce antinociception in neuropathic pain conditions because of its action on the PLCgamma-1/CREB-signaling pathway. Imipramine 46-56 cAMP responsive element binding protein 1 Mus musculus 165-169 17487276-8 2007 Treatment of the stressed mice with the antidepressant imipramine normalized luciferase expression to control levels in all brain regions and likewise reduced CREB-phosphorylation. Imipramine 55-65 cAMP responsive element binding protein 1 Mus musculus 159-163 16519925-6 2006 Repeated treatment with antidepressant drugs, imipramine (Imi) and fluoxetine (Flu), significantly reduced the plasma corticosterone concentration and enhanced the BDNF and CREB levels. Imipramine 46-56 cAMP responsive element binding protein 1 Mus musculus 173-177 16519925-6 2006 Repeated treatment with antidepressant drugs, imipramine (Imi) and fluoxetine (Flu), significantly reduced the plasma corticosterone concentration and enhanced the BDNF and CREB levels. Imipramine 58-61 cAMP responsive element binding protein 1 Mus musculus 173-177