Browsing by Author "Büyükuysal, Rifat Levent"
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Item Choline as an agonist - determination of its agonistic potency on cholinergic receptors(Pergamon-Elsevier Science Ltd, 1998) Millington, William; Kıran, Burhan K.; Ulus, İsmail H.; Büyükuysal, Rifat Levent; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; D-5340-2015; AAH-1652-2021; 7004830308; 7004271086; 6602686612These experiments examined the potency of choline as a cholinergic agonist at both muscarinic and nicotinic receptors in rat brain and peripheral tissues. Choline stimulated the contraction of isolated smooth muscle preparations of the stomach fundus, urinary bladder and trachea and reduced the frequency of spontaneous contractions of the right atrium at high micromolar and low millimolar concentrations. The potency of choline to elicit a biological response varied markedly among these tissues; ec50 values ranged between 0.41 mM in the fundus to 14.45 mM in the atrium. Choline also displaced [3H]quinuclidinyl benzilate binding in a concentration-dependent manner although, again, its potency varied among different brain regions (Ki = 1.2 to 3.5 mM) and peripheral tissues (Ki = 0.28 to 3.00 (mM). Choline exhibited a comparable affinity for nicotinic receptors. It stimulated catecholamine release from the vascularly perfused adrenal gland () and displaced l-[3H]nicotine binding to membrane preparations of brain and peripheral tissues (Ki = 0.38 to 1.17mM). However, the concentration of choline required to bind to cholinergic receptors in most tissues was considerably higher than serum levels either in controls (8–13 μM) or following the administration of choline chloride (200 μM). These results clearly demonstrate that choline is a weak cholinergic agonist. Its potency is too low to account for the central nervous system effects produced by choline administration, although the direct activation of cholinergic receptors in several peripheral tissues may explain some of its side effects.Item Effects of ketamine and thiopental on ischemia reoxygenation-induced LDH leakage and amino acid release from rat striatal slices(Lippincott Williams & Wilkins, 2005-01) Başağan Moğol, Elif; Büyükuysal, Rifat Levent; Korfalı, Gülsen; Uludağ Üniversitesi/Tıp Fakültesi/Anestezi ve Reanimasyon Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı.; AAH-1657-2021; 23982134100; 6602686612; 6701462594Increased release of glutamate is thought to contribute to ischemia-induced neuronal damage. Since general anesthetics such as thiopental and ketamine are thought to provide some degree of cerebral protection, this study was intended to 1) compare the effectiveness of ketamine and thiopental on ischemia-induced tissue damage; and, if so, 2) determine whether attenuation of the increased amino acid release is the sole mechanism for the protective effects demonstrated. Striatal slices prepared from Wistar Albino rats were incubated in an ischemic medium for 1 hour followed by 5 hours in a reoxygenation (REO) medium. Ketamine and thiopental were added medium during ischemia and/or REO periods, and the medium was collected at the end of each incubation period for measurement of amino acid release and lactate dehydrogenase (LDH) leakage. Ischemia significantly increased amino acid release without altering LDH leakage. Ischemia-induced increments in glutamate and aspartic acid releases returned to control levels during REO, but LDH leakage increased (P < 0.001) during this period. Although ketamine (100 muM) and thiopental (100 mu\M) failed to decrease ischermia-induced excitatory amino acid release, they protected the slices against REO-induced LDH leakage. Ketamine, but not thiopental, was effective even if added after ischemia (P < 0.05). These results indicate that ketamine and thiopental protect the slices against REO-induced LDH leakage. However, mechanisms other than attenuation of the enhanced glutamate release might be responsible for their protective effects.Item Protein S100B release from rat brain slices during and after ischemia: Comparison with lactate dehydrogenase leakage(Pergamon-Elsevier Science, 2005-12) Büyükuysal, Rifat Levent; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı.; AAH-1657-2021; 6602686612One hour of ischemia significantly increased protein S100B release from rat brain slices without altering lactate dehydrogenase leakage. Reoxygenation of the ischemic slices, however, increased the levels of these biochemical markers in the medium. Although removal of extracellular Ca+2 ions from the medium did not alter the basal lactate dehydrogenase leakage from cortical slices, an excessive increase in basal protein S100B release was seen under this condition. Ischemia and/or reoxygenation induced enhancements in these markers were attenuated by removal of Ca+2 ions from the medium. Ischemia significantly increased glutamate release, but neither ischernia nor reoxygenation induced rises in protein S100B and lactate dehydrogenase levels were altered by glutamate receptor antagonists. Rising the glutamate levels in the medium by each ouabain or exogenous glutamate, moreover, failed in exerting an ischernia like effect on protein S100B and LDH outputs. In contrast, exogenous glutamate added into the medium protected the slices against reoxygenation induced increments in protein S100B and lactate dehydrogenase levels. These results indicate that protein S100B has a greater sensitivity against ischernia than lactate dehydrogenase in in vitro brain slice preparations. Since neither exogenous glutamate nor enhancements of the extracellular glutamate levels by ouabain had an ischemia like effect, and since glutamate receptor antagonists were also unsuccessful, it seems unlikely that ischemia-induced increase in glutamate release is directly involved in protein S100B release or lactate dehydrogenase leakage determined in the present study.Item Resveratrol protects rat striatal slices against anoxia-induced dopamine release(Springer, 2008-09) Gürsoy, Murat; Büyükuysal, Rifat Levent; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı.; AAH-1657-2021; 57197640824; 6602686612Incubation of rat striatal slices in anoxic medium caused significant alterations in dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) outputs; while DA release increased several times, 50% decline in DOPAC output was observed under this condition. Tissue ATP level, on the other hand, was decreased 40% by anoxia. Presence of resveratrol in the medium decreased anoxia-induced DA release in a concentration-dependent manner. Enhanced DA output, however, was declined slightly by epicatechine and catechine, and not altered significantly by morin hydrate and quercetin dehydrate which are other penolic compounds present in the red wine. In contrary to DA output, anoxia-induced decline in tissue ATP level was not ameliorated by resveratrol. In addition to anoxia, resveratrol, as observed with DA uptake blocker nomifensine, also reduced DA release stimulated by ouabain. Efficiencies of both resveratrol and nomifensine to attenuate ouabain-induced DA output, however, were closely dependent on ouabain concentration in the medium. These results indicate that some phenolic compounds, particularly resveratrol decrease anoxia-induced DA output and appear promising agents to improve the alterations occurred under anoxic-ischemic conditions.