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Antidepressant-like and anxiolytic-like activity of a novel indoleamine derivative ADN -2013 in rodents

100%
Wasik A., Partyka A., Jastrzębska-Więsek M., Kołaczkowski M., Wesołowska A.
Medicina Internacia Revuo
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2017
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vol. 28
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issue 108
152-162
EN
A novel indolamine derivative, ADN-2013, has been proved to possess a preclinical activity profile appropriate for the treatment of behavioral and psychological symptoms of dementia. Its antidepressant and anxiolytic properties have been examined in rat and mice models. The receptor mechanisms underlying the antidepressant properties of ADN-2013 have also been elucidated. ADN-2013 significantly shortened the immobility time measured in the forced swim test in mice and rats, producing an effect that was abolished by the dopamine D1-receptor antagonist SCH 23390 in rats. Moreover, ADN-2013 evoked anxiolytic-like activity in both “conditional” and “unconditional” anxiety-like paradigms in mice and rats. From these results, it is likely that direct antagonism toward serotonin 5-HT6 receptors and an indirect effect of dopamine, acting mostly via D1-like receptors, may be involved in the antidepressant action of ADN-2013. However, the partial agonist activity of ADN-2013 toward D2 receptors, observed in in vitro studies, might also contribute to this effect.
2
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Is MLC phosphorylation essential for the recovery from ROCK inhibition in glioma C6 cells?

86%
Korczyński J., Sobierajska K., Krzemiński P., Wasik A., Wypych D., Pomorski P., Kłopocka W.
Acta Biochimica Polonica
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2011
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vol. 58
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issue 1
125-130
EN
Inhibition of Rho-associated protein kinase (ROCK) activity in glioma C6 cells induces changes in actin cytoskeleton organization and cell morphology similar to those observed in other types of cells with inhibited RhoA/ROCK signaling pathway. We show that phosphorylation of myosin light chains (MLC) induced by P2Y2 receptor stimulation in cells with blocked ROCK correlates in time with actin cytoskeleton reorganization, F-actin redistribution and stress fibers assembly followed by recovery of normal cell morphology. Presented results indicate that myosin light-chain kinase (MLCK) is responsible for the observed phosphorylation of MLC. We also found that the changes induced by P2Y2 stimulation in actin cytoskeleton dynamics and morphology of cells with inhibited ROCK, but not in the level of phosphorylated MLC, depend on the presence of calcium in the cell environment.
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