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Öğe Assessing the effects of the neonicotinoid insecticide imidacloprid in the cholinergic synapses of the stellate cells of the mouse cochlear nucleus using whole-cell patch-clamp recording(Elsevier Science Bv, 2010) Bal, Ramazan; Erdogan, Suat; Theophilidis, George; Baydas, Giyasettin; Naziroglu, MustafaImidacloprid (IMI) is widely used systemic insecticide that acts as an agonist on nicotinic acetylcholine receptors (nAChRs). IMI has been reported to be more active against insect nAChRs (EC(50) 0.86-1 mu M) than it is against mammalian nAChRs (EC(50) 70 mu M). The objective of this study was to determine to what extent IMI affects the nAChRs of the stellate cells of mouse cochlear nucleus (CN), using whole-cell patch-clamp recording. Puff application of 1 mu M IMI had no significant effect on the membrane properties of the neurons tested, while a concentration of 10 mu M caused a significant depolarizing shift in the membrane potential and resulted in increases in the fluctuation of the membrane potential and in the frequency of miniature postsynaptic potentials (mpps) within less than a minute of exposure. IMI at concentrations >= 50 mu M caused a significant depolarizing shift in the membrane potential, accompanied by a marked increase in the frequency of action potential. IMI decreased the membrane input resistance and the membrane time constants. Bath application of 50 mu M d-tubocurarine (d-TC) reversibly blocked the depolarizing shift of the resting membrane potential and the spontaneous firing induced by IMI application in Current clamp and blocked the inward Currents through nicotinic receptors induced by IMI application in voltage clamp. Similarly, 100 nM alpha-bungarotoxin (alpha-BgTx) blocked the spontaneous firing induced by IMI (n = 3). The amplitude of the 100 mu M IMI-induced inward current at -60 mV holding potential was 115.0 +/- 16.2 pA (n = 7). IMI at a concentration of 10 mu M produced 11.3 +/- 3.4 pA inward current (n = 4). We conclude that exposure to IMI at concentrations >= 10 mu M for <1 min can change the membrane properties of neurons that have nAChRs and. as a consequence, their function. (C) 2009 Elsevier Inc. All rights reserved.Öğe Ceftriaxone ameliorates cyclosporine A-induced oxidative nephrotoxicity in rat(Wiley, 2011) Yilmaz, Nigar; Ilhan, Selcuk; Naziroglu, Mustafa; Oktar, Suleyman; Nacar, Ahmet; Arica, Vefik; Tutanc, MuratA growing body of evidence now suggested that cyclosporine A (CycA)-induced nephrotoxicity is a crucial clinical problem and oxidative stress is importantly responsible for its toxicity. Ceftriaxone induced antioxidant effect in brain and neuronal tissues against oxidative damage although its antioxidant potential effect on kidney has not been clarified. The aim of this study was to evaluate whether ceftriaxone protects CycA-induced oxidative stress kidney injury in rats. Twenty-four rats were equally divided into four groups. First group was used as control. Ceftriaxone (200 mg/kg) and CycA (15 mg/kg) were administrated to second and third groups for 10 days, respectively. The ceftriaxone and CycA combination was given to rats constituting the fourth group for 10 days. Lipid peroxidation (LP), urea nitrogen and lactate dehydrogenase (LDH) levels were higher in CycA group than in control and ceftriaxone groups although LP, urea nitrogen and LDH levels were lower in ceftriaxone + CycA group than in control and ceftriaxone groups. Glutathione peroxidase and catalase activities were lower in CycA group than in control whereas their activities were increased in control and ceftriaxone groups. Superoxide dismutase activity did not change by the treatments. Ceftriaxone administration recovered also CycA-induced atrophy, vacuolization and exfoliations of tubular epithelium and glomerular collapse in histopathological evaluation of kidney. In conclusion, we observed that ceftriaxone is beneficial on CycA-induced oxidative stress in kidney of rats by modulating oxidative and antioxidant system. Copyright (C) 2011 John Wiley & Sons, Ltd.Öğe Morphine Induces Apoptosis, Inflammation, and Mitochondrial Oxidative Stress via Activation of TRPM2 Channel and Nitric Oxide Signaling Pathways in the Hippocampus(Springer, 2020) Osmanloglu, Omer; Yldirim, Mustafa Kemal; Akyuva, Yener; Yildizhan, Kenan; Naziroglu, MustafaMorphine as an opioid is an important drug in the treatment of moderate to severe pain. Several stress factors via generation of nitric oxide (NO) and oxidative stress (OS) are responsible for the adverse effects of morphine-induced analgesia, addiction, and antinociceptive tolerance, including altered Ca(2+)concentration, inflammation, OS, and release of apoptotic factors. TRPM2 is a Ca2+-permeable cation channel and it is activated by OS and NO. Hence, adverse effect of morphine addiction may occur via the OS and NO-induced TRPM2 activation. Because of the unclear etiology of morphine-induced adverse effects in the hippocampus, investigating the involvement of TRPM2 and NO synthetase (NOS) activations in the treatment of morphine-induced OS, apoptosis, and neuroinflammation is a major challenge. The hippocampal neuron of TRPM2 wild-type (TRPM2-WT) and knockout (TRPM2-KO) mice were divided into control, morphine, NOS inhibitor (L-NAME) + morphine, and TRPM2 channel blockers (ACA and 2-APB) + morphine. The morphine-induced increases of apoptosis, neuron death, OS, lipid peroxidation, caspase-3 and caspase-9, neuroinflammatory cytokines (IL-1 beta, TNF-alpha, IL-6), and Ca(2+)levels in the hippocampal neuron of TRPM2-WT mouse were decreased by the L-NAME, ACA, and 2-APB treatments, although cell viability, neuron count, and reduced glutathione and glutathione peroxidase levels were increased by the treatments. However, the effects of morphine were not observed in the hippocampus of TRPM2-KO mice. Taken together, our data show that neurodegeneration adverse effects of morphine were induced by activation of TRPM2, and excessive generations of NO and OS. Thus, inhibition of TRPM2 may modulate morphine-induced neurodegeneration in the hippocampus.Öğe Morphine Induces Apoptosis, Inflammation, and Mitochondrial Oxidative Stress via Activation of TRPM2 Channel and Nitric Oxide Signaling Pathways in the Hippocampus (vol 17, pg 313, 2020)(Springer, 2020) Osmanlioglu, Haci Omer; Yildirim, Mustafa Kemal; Akyuva, Yener; Yildizhan, Kenan; Naziroglu, Mustafa[Abstract Not Available]Öğe Resveratrol attenuates hypoxia-induced neuronal cell death, inflammation and mitochondrial oxidative stress by modulation of TRPM2 channel(Nature Portfolio, 2020) Akyuva, Yener; Naziroglu, MustafaHypoxia (HYPX) induced-overload Ca2+ entry results in increase of mitochondrial oxidative stress, inflammation and apoptosis in several neurons. Ca2+ permeable TRPM2 channel was gated by ADPribose (ADPR) and reactive oxygen species (ROS), although its activity was modulated in HYPX-exposed neurons by resveratrol (RSV). The aim of this study was to evaluate if a therapy of RSV can modulate the effect of HYPX in the TRPM2 expressing SH-SY5Y neuronal and HEK293 (no expression of TRPM2) cell lines. The SH-SY5Y and HEK293 cells were divided into four groups as control, RSV (50 mu M and 24 hours), and HYPX and RSV + HYPX. For induction of HYPX in the cells, CoCl2 (200 mu M and 24 hours) incubation was used. HYPX-induced intracellular Ca2+ responses to TRPM2 activation were increased in the SH-SY5Y cells but not in the HEK293 cells from coming H2O2 and ADPR. RSV treatment improved intracellular Ca2+ responses, mitochondrial function, suppressed the generation of cytokine (IL-1 beta and TNF-alpha), cytosolic and mitochondrial ROS in the SH-SY5Y cells. Intracellular free Zn2+, apoptosis, cell death, PARP-1, TRPM2 expression, caspase -3 and -9 levels are increased through activating TRPM2 in the SH-SY5Y cells exposed to the HYPX. However, the values were decreased in the cells by RSV and TRPM2 blockers (ACA and 2-APB). In SH-SY5Y neuronal cells exposed to HYPX conditions, the neuroprotective effects of RSV were shown to be exerted via modulation of oxidative stress, inflammation, apoptosis and death through modulation of TRPM2 channel. RSV could be used as an effective agent in the treatment of neurodegeneration exposure to HYPX.Öğe Selenium prevents interferon-gamma induced activation of TRPM2 channel and inhibits inflammation, mitochondrial oxidative stress, and apoptosis in microglia(Springer/Plenum Publishers, 2021) Akyuva, Yener; Naziroglu, Mustafa; Yildizhan, KenanMicroglia as the primary immune cells of brain act protective effects against injuries and infections in the central nervous system. Inflammation via excessive Ca(2+)influx and oxygen radical species (ROS) generation is a known factor in many neurodegenerative disorders. Importantly, the Ca(2+)permeable TRPM2 channel is activated by oxidative stress. Thus, TRPM2 could provide the excessive Ca(2+)influx in the microglia. Although TRPM2 expression level is high in inflammatory cells, the interplay between mouse microglia and TRPM2 channel during inflammation is not fully identified. Thus, it is important to understand the mechanisms and factors involved in order to enhance neuronal regeneration and repair. The data presented here indicate that TRPM2 channels were activated in microglia cells by interferon-gamma (IFN gamma). The IFN gamma treatment further increased apoptosis (early and late) and cytokine productions (TNF-alpha, IL-1 beta, and IL-6) which were due to increased lipid peroxidation and ROS generations as well as increased activations of caspase -3 (Casp-3) and - 9 (Casp-9). However, selenium treatment diminished activations of TRPM2, cytokine, Casp-3, and Casp-9, and levels of lipid peroxidation and mitochondrial ROS production in the microglia that were treated with IFN gamma. Moreover, addition of either PARP1 inhibitors (PJ34 or DPQ) or TRPM2 blockers (2-APB or ACA) potentiated the modulator effects of selenium. These results clearly suggest that IFN gamma leads to TRPM2 activation in microglia cells; whereas, selenium prevents IFN gamma-mediated TRPM2 activation and cytokine generation. Together the interplay between IFN gamma released from microglia cells is importance in brain inflammation and may affect oxidative cytotoxicity in the microglia.
