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GÖREN, MEHMET ZAFER

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GÖREN

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MEHMET ZAFER

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  • Publication
    Contribution of M-1 and M-2 muscarinic receptor subtypes to convulsions in fasted mice treated with scopolamine and given food
    (ELSEVIER SCIENCE BV, 2019) AYDIN OMAY, BANU; Bacanak, Merve Saygi; Aydin, Banu; Cabadak, Hulya; Nurten, Asiye; Goren, Mehmet Zafer; Enginar, Nurhan
    Treatment of fasted mice and rats with the nonselective muscarinic antagonist, scopolamine or atropine, causes convulsions after food intake. This study evaluated the effect of fasting on the expression of M-1 and M-2 muscarinic receptors in the brain regions, the relationship between receptor expression and seizure stages, and the muscarinic receptor subtype which plays a role in the occurrence of convulsions. Mice were grouped as allowed to eat ad lib (fed) and deprived of food for 24 h (fasted). Fasted animals developed convulsions after being treated with scopolamine (60%) or the selective M-1 receptor antagonist pirenzepine (10 mg/kg; 20% and 60 mg/kg; 70%) and given food. Fasting increased expression of M-1 receptors in the frontal cortex and M-2 receptors in the hippocampus, but produced no change in the expression of both receptors in the amygdaloid complex. Food intake after fasting decreased M-1 receptor expression in the frontal cortex and M-1 and M-2 receptor expression in the hippocampus. Seizure severity was uncorrelated with muscarinic receptor expression in the brain regions. Taken together, these findings provide evidence for the role of M-1 muscarinic receptor antagonism and fasting-induced increases in M-1 and M-2 expression possible underlying mechanism in the occurrence of convulsions in fasted animals.
  • Publication
    Investigation of the Roles of Non-neuronal Acetylcholine in Chronic Myeloid Leukemic Cells and their Erythroid or Megakaryocytic Differentiated Lines
    (BENTHAM SCIENCE PUBL LTD, 2018) AYDIN OMAY, BANU; Aydin, Banu; Cabadak, Hulya; Goren, M. Zafer
    Background: Many studies suggested that Acetylcholine (ACh) might serve as an autocrine/paraerine growth factor in several types of tumors or tumor cell lines. High levels of Acetylcholinesterase (AChE) activity have been reported in primary brain tumors, ovarian, colon and lung tumors. Objectives: The role of cholinergic signaling needs to be clarified in in leukemia. Method: K562 cells were derived from a chronic myelogenous leukemia patient during blast crisis serving as pluripotent hematopoietic stein cells. K562 cells were incubated with various cholinergic agonists or antagonists to investigate the role of ACh in different differentiated cell lines. Results: Our experiments showed that AChE activity was increased in response to ACh in undifferentiated K562 cells, but in the erythroid differentiated K562 cells a high concentration of ACh (1 mM) decreased the AChE activity. ACh failed to elevate the AChE activity in the megakaryocytic differentiated K562 cells. An AChE inhibitor, eserine, also suppressed the AChE activity in a concentration-dependent manner. Choline uptake inhibition by hemicholinium did increase the AChE activity but not in the erythroid differentiated K562 DOS cell line. Likewise, megakaryocytic differentiated K562 cells also displayed a similar pattern. Vesamicole, a vesicular choline uptake inhibitor, produced similar results. Curare, a nicotinic antagonist, elevated the cell counts of the megakaryocytic differentiated cells. Conclusion: Our findings may suggest excess extracellular ACh will decrease the cell growth in undifferentiated and megakaryocytic differentiated K562 cell lines through nicotinic type cholinoceptors.