المساهمون: Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı., Büyükuysal, Rifat Levent, AAH-1657-2021, 6602686612

مصطلحات موضوعية: Protein S100B, Lactate dehydrogenase leakage, Ischemia, Amino-acid release, Oxygen, Glucose deprivation, Molecular-mechanisms, Hippocampal slices, Glutamate release, NA+/CA2+ channel, Hypoxic injury, Growth-factor, Damage, Biochemistry & molecular biology, Neurosciences & neurology, Animals, Brain, Brain ischemia, Calcium, Disease models, Animal, Energy metabolism, Enzyme inhibitors, Excitatory amino acid antagonists, Glutamic acid, L-Lactate dehydrogenase, Nerve growth factors, Neurons, Organ culture techniques, Ouabain

الوصف: One 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.

العلاقة: Makale - Uluslararası Hakemli Dergi; Neurochemistry International; Büyükuysal, R. L. (2005). "Protein S100B release from rat brain slices during and after ischemia: Comparison with lactate dehydrogenase leakage". Neurochemistry International, 47(8), 580-588.; https://doi.org/10.1016/j.neuint.2005.06.009Test; http://hdl.handle.net/11452/21281Test; 000232968500008; 2-s2.0-26444602562; 580; 588; 47

الإتاحة: https://doi.org/10.1016/j.neuint.2005.06.009Test
http://hdl.handle.net/11452/21281Test

المساهمون: Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı., Büyükuysal, Rifat Levent, AAH-1657-2021, 6602686612

مصطلحات موضوعية: Protein S100B, Lactate dehydrogenase leakage, Ischemia, Amino-acid release, Oxygen, Glucose deprivation, Molecular-mechanisms, Hippocampal slices, Glutamate release, NA+/CA2+ channel, Hypoxic injury, Growth-factor, Damage, Biochemistry & molecular biology, Neurosciences & neurology, Animals, Brain, Brain ischemia, Calcium, Disease models, Animal, Energy metabolism, Enzyme inhibitors, Excitatory amino acid antagonists, Glutamic acid, L-Lactate dehydrogenase, Nerve growth factors, Neurons, Organ culture techniques, Ouabain

الوصف: One 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.

العلاقة: Makale - Uluslararası Hakemli Dergi; Neurochemistry International; Büyükuysal, R. L. (2005). "Protein S100B release from rat brain slices during and after ischemia: Comparison with lactate dehydrogenase leakage". Neurochemistry International, 47(8), 580-588.; https://doi.org/10.1016/j.neuint.2005.06.009Test; http://hdl.handle.net/11452/21281Test; 000232968500008; 2-s2.0-26444602562; 580; 588; 47

الإتاحة: https://doi.org/10.1016/j.neuint.2005.06.009Test
http://hdl.handle.net/11452/21281Test

المساهمون: Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı., Gürsoy, Murat, Büyükuysal, Rıfat Levent, AAH-1657-2021, 57197640824, 6602686612

مصطلحات موضوعية: S100B release, Oxygen-glucose deprivation (OGD), Re-oxygenation, Protein-kinase-C, Delayed neuronal injury, In-vitro trauma, Cerebral-ischemia, Brain-slices, Hippocampal-neurons, Damage, Secretion, Glutamate, Toxicity, Biochemistry & molecular biology, Neurosciences & neurology, Rattus, Animals, Calcium channel blockers, Cerebral cortex, Enzyme activation, Enzyme inhibitors, Female, Glucose, Glutamic acid, Hypoxia, brain, Ketoglutaric acids, L-lactate dehydrogenase, Male, Nerve growth factors

الوصف: Incubation of rat cortical slices in a medium that was not containing oxygen and glucose (oxygen-glucose deprivation, OGD) caused a 200% increase in the release of S100B. However, when slices were transferred to a medium containing oxygen and glucose (reoxygenation conditions, or REO), S100B release reached 500% of its control value. Neither inhibition of nitric oxide (NO) synthase by L-NAME nor addition of the NO donors sodium nitroprussid (SNP) or hydroxylamine (HA) to the medium altered basal S100B release. Similarly, the presence of SNP, HA or NO precursor l-arginine in the medium, or inhibition of NO synthase by L-NAME also failed to alter OGD- and REO-induced S100B outputs. Moreover, individual inhibition of PKC, PLA(2) or PLC all failed to attenuate the S100B release determined under control condition or enhanced by either OGD or REO. Blockade of calcium channels with verapamil, chelating the Ca+2 ions with BAPTA or blockade of sodium channels with tetrodotoxin (TTX) did not alter OGD- and REO-induced S100B release. In contrast to the pharmacologic manipulations mentioned above, glutamate and alpha-ketoglutarate added at high concentrations to the medium prevented both OGD- and REO-induced S100B outputs. These results indicate that neither NO nor the activation of PKC, PLA(2) or PLC seem to be involved in basal or OGD- and REO-induced S100B outputs. Additionally, calcium and sodium currents that are sensitive to verapamil and TTX, respectively, are unlikely to contribute to the enhanced S100B release observed under these conditions.

العلاقة: Makale - Uluslararası Hakemli Dergi; 2006/49; Neurochemical Research; Gürsoy, M. ve Büyükuysal, R. L. (2010). "Mechanism of S100b release from rat cortical slices determined under basal and stimulated conditions". Neurochemical Research, 35(3), 429-436.; https://doi.org/10.1007/s11064-009-0075-9Test; https://link.springer.com/article/10.1007/s11064-009-0075-9Test; http://hdl.handle.net/11452/25400Test; 000274403600010; 2-s2.0-76849087262; 429; 436; 35

الإتاحة: https://doi.org/10.1007/s11064-009-0075-9Test
http://hdl.handle.net/11452/25400Test

المساهمون: Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı., Gürsoy, Murat, Büyükuysal, Rıfat Levent, AAH-1657-2021, 57197640824, 6602686612

مصطلحات موضوعية: S100B release, Oxygen-glucose deprivation (OGD), Re-oxygenation, Protein-kinase-C, Delayed neuronal injury, In-vitro trauma, Cerebral-ischemia, Brain-slices, Hippocampal-neurons, Damage, Secretion, Glutamate, Toxicity, Biochemistry & molecular biology, Neurosciences & neurology, Rattus, Animals, Calcium channel blockers, Cerebral cortex, Enzyme activation, Enzyme inhibitors, Female, Glucose, Glutamic acid, Hypoxia, brain, Ketoglutaric acids, L-lactate dehydrogenase, Male, Nerve growth factors

الوصف: Incubation of rat cortical slices in a medium that was not containing oxygen and glucose (oxygen-glucose deprivation, OGD) caused a 200% increase in the release of S100B. However, when slices were transferred to a medium containing oxygen and glucose (reoxygenation conditions, or REO), S100B release reached 500% of its control value. Neither inhibition of nitric oxide (NO) synthase by L-NAME nor addition of the NO donors sodium nitroprussid (SNP) or hydroxylamine (HA) to the medium altered basal S100B release. Similarly, the presence of SNP, HA or NO precursor l-arginine in the medium, or inhibition of NO synthase by L-NAME also failed to alter OGD- and REO-induced S100B outputs. Moreover, individual inhibition of PKC, PLA(2) or PLC all failed to attenuate the S100B release determined under control condition or enhanced by either OGD or REO. Blockade of calcium channels with verapamil, chelating the Ca+2 ions with BAPTA or blockade of sodium channels with tetrodotoxin (TTX) did not alter OGD- and REO-induced S100B release. In contrast to the pharmacologic manipulations mentioned above, glutamate and alpha-ketoglutarate added at high concentrations to the medium prevented both OGD- and REO-induced S100B outputs. These results indicate that neither NO nor the activation of PKC, PLA(2) or PLC seem to be involved in basal or OGD- and REO-induced S100B outputs. Additionally, calcium and sodium currents that are sensitive to verapamil and TTX, respectively, are unlikely to contribute to the enhanced S100B release observed under these conditions.

العلاقة: Makale - Uluslararası Hakemli Dergi; 2006/49; Neurochemical Research; Gürsoy, M. ve Büyükuysal, R. L. (2010). "Mechanism of S100b release from rat cortical slices determined under basal and stimulated conditions". Neurochemical Research, 35(3), 429-436.; https://doi.org/10.1007/s11064-009-0075-9Test; https://link.springer.com/article/10.1007/s11064-009-0075-9Test; http://hdl.handle.net/11452/25400Test; 000274403600010; 2-s2.0-76849087262; 429; 436; 35

الإتاحة: https://doi.org/10.1007/s11064-009-0075-9Test
http://hdl.handle.net/11452/25400Test