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Search Results: 1 - 10 of 285 matches for " Lidija Radenovi? "
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Effect of 7-nitroindazoleon superoxide production and MnSOD activity in threat brain following kainate-induced neurotoxicity
RadenoviLidija
Archives of Biological Sciences , 2008, DOI: 10.2298/abs0801025r
Abstract: We investigated the effect of 7-nitroindazole (7-NI), a selective neuronal nitric oxide synthase inhibitor in vivo, on superoxide concentration as well its influence on mitochondrial MnSOD activity since this activity is associated with the production of reactive oxygen species after kainate-induced neurotoxicity. The time course of in vivo oxidative damage in different brain regions was investigated. Measurements were performed at different times (5 min, 15 min, 2 h, 48 h, and 7 days) in the ipsi- and contralateral hippocampus, forebrain cortex, striatum, and cerebellum homogenates. Our results indicated that 7-NI had no statistically significant influence on superoxide concentrations in the tested brain structures compared to the control values. However, superoxide concentrations after kainate-induced neurotoxicity returned to the control values after pretreatment with 7-NI in all tested brain structures. Regarding the activity of MnSOD, our results demonstrated statistically significant increase 7 days after intrahippocampal KA treatment in all tested brain structures after pretreatment with 7-NI. The obtained results suggest that neuronal NO synthase inhibitors may be useful in the treatment of neurological diseases in which excitotoxic mechanisms play a role.
Mitochondrial superoxide production and MnSOD activity following exposure to an agonist and antagonists of ionotropic receptors in rat brain
RadenoviLidija Lj.,Selakovi? Vesna
Archives of Biological Sciences , 2005, DOI: 10.2298/abs0501001r
Abstract: The involvement of NMDA and AMPA/kainate receptors in the induction of superoxide production in the rat brain was examined after intrahippocampal injection of kainate, a non-NMDA receptor agonist; kainate plus CNQX, a selective AMPA/kainate receptor antagonist; or kainate plus APV, a selective NMDA receptor antagonist. The measurements took place at different times in the ipsi- and contralateral hippocampus, forebrain cortex, striatum, and cerebellum homogenates. The used glutamate antagonists both ensured sufficient neuroprotection in the sense of lowering superoxide production and raising MnSOD levels, but in the mechanisms and time dynamics of their effects were different. Our findings suggest that NMDA and AMPA/kainate receptors are differentially involved in superoxide production. UDC 612.815 612.82.
Kainate-induced oxidative stress and neurotoxicity in the rat brain
RadenoviLidija Lj.,Selakovi? Vesna
Archives of Biological Sciences , 2005, DOI: 10.2298/abs0504259r
Abstract: We investigated superoxide production and MnSOD activity after kainate injection into the CA3 region of the rat hippocampus. The measurements took place at different times in hippocampus, forebrain cortex, striatum, and cerebellum homogenates. Free radicals including superoxide are responsible for post-lesional cytotoxicity. Neuronal cells responded to oxidative stress in kainate-induced neurotoxicity and caused the protective mechanism to increase MnSOD levels. The increase of MnSOD in distinct brain regions functionally connected via afferents and efferent suggests that these regions are affected by the injury. It implies that MnSOD protects the cells in these regions from superoxide-induced damage and therefore may limit the retrograde and anterograde spread of neurotoxicity.
Modification of the acetylcholine-induced current of the snail Helix pomatia L. by fast temperature changes
Nedeljkovi? M.,Kartelija Gordana,RadenoviLidija
Archives of Biological Sciences , 2005, DOI: 10.2298/abs0503181n
Abstract: Using the single electrode voltage clamp method, we found that acetylcholine (aCh) induces transient inward dose-dependent current on the membrane of the identified Helix pomatia Br neuron. We analyzed the effects of fast cooling and heating as well as thermal acclimation on the aCh inward current. the experiments were conducted on active and dormant snails acclimated to either 20 or 7°C for at least four weeks. the Hill coefficient remained approximately 1 in all cases, which means that there is a single aCh binding site on the membrane. Fast temperature alternations induce binding affinity changes. in the work presented, we analyzed the effects of cooling on the aCh-induced inward current. the amplitude of aCh-induced inward current was markedly reduced after cooling, and the speed of decay of the aCh response was lower.
Photosensitive neurons in mollusks
Kartelija Gordana,Nedeljkovi? M.,RadenoviLidija Lj.
Archives of Biological Sciences , 2005, DOI: 10.2298/abs0504247k
Abstract: In addition to regular photoreceptors, some invertebrates possess simple extra ocular photoreceptors. For ex-ample, the central ganglia of mollusks contain photosensitive neurons. These neurons are located on the dorsal surface of the ganglia and based on their electrophysiological properties it has been postulated that they are internal photoreceptors. Besides the eye, transduction of light also occurs in these extra-ocular photoreceptors. In the present work, we analyze the reactivity of these nerve cells to light and describe the underlying mechanism mediating the light-induced response.
Neuroprotectionby MK-801 following cerebral ischemia in Mongolian gerbils
RadenoviLidija,Selakovi? Vesna,An?us P.R.
Archives of Biological Sciences , 2008, DOI: 10.2298/abs0803341r
Abstract: Global cerebral ischemia in Mongolian gerbils is an established model in experimental research on cerebral ischemia, which is characterized morphologically by selective neuronal damage in the hippocampus, striatum, and cortex. Elevated glutamate levels are thought to be a primary cause of neuronal death after global cerebral ischemia. The purpose of this study was to investigate the potential neuroprotective effects of dizocilpine malate (MK-801), a non-competitive glutamate antagonist, in the model of 10-min gerbil cerebral ischemia. Gerbils were given MK-801(3 mg/kg i.p.)or saline immediately after the occlusion. On day 4 after reperfusion, neuronal damage was examined in the hippocampus (30 μm)and striatum slices (5 μm)stained with hematoxylin/eosin, fluorescent Nissl staining and membrane tracer DiI. The striatum and C3 regions of the hippocampus were analyzed by confocal microscopy. Neuroprotection was determined by quantifying the degree of cell loss, reduction of morphologically damaged cells, and the degree of preservation of recog-nizable neuroanatomical pathways after the ischemic insult. Our results demonstrate that the neuronal damage induced by sustained ischemia is related to abnormalities in glutamatergic function associated with NMDA receptors. MK-801significantly prevented neuronal loss in the tested brain structures. All of this contributes to a better understanding of the given pathophysiological process causing ischemic neuronal damage.
7-nitroindazole, a selective neuronal nitric oxide synthase inhibitore in vivo, prevents kainate-induced intrahippocampal neurotoxicity
RadenoviLidija Lj.,Selakovi? Vesna,Bo?i? Biljana
Archives of Biological Sciences , 2005, DOI: 10.2298/abs0502075r
Abstract: We investigated the effects of 7-nitroindazole (7-NI), a selective neuronal nitric oxide synthase inhibitor in vivo, on nitrite concentration after kainic acid injection unilaterally into the CA3 region of the rat hippocampus. The accumulation of nitrite, the stable metabolite of NO, was measured by the Griess reaction at different times in hippocampus, forebrain cortex, striatum, and cerebellum homogenates. 7-nitroindazole can effectively inhibit NO synthesis in rat brain after kainate-induced neurotoxicity and suppressed nitrite accumulation. The present results suggest that neuronal NO synthase inhibitors may be useful in the treatment of neurological diseases in which excitotoxic mechanisms play a role.
Effect of glutamate antagonists on nitric oxide production in rat brain following intrahippocampal injection
RadenoviLidija,Selakovi? Vesna,Jana? Branka,Todorovi? Dajana
Archives of Biological Sciences , 2007, DOI: 10.2298/abs0701029r
Abstract: Stimulation of glutamate receptors induces neuronal nitric oxide (NO) release, which in turn modulates glutamate transmission. The involvement of ionotropic glutamate NMDA and AMPA/kainate receptors in induction of NO production in the rat brain was examined after injection of kainate, a non-NMDA receptor agonist; kainate plus 6-cyano- 7-nitroquinoxaline-2,3-dione (CNQX), a selective AMPA/kainate receptor antagonist; or kainate plus 2-amino-5-phosphonopentanoic acid (APV), a selective NMDA receptor antagonist. Competitive glutamate receptor antagonists were injected with kainate unilaterally into the CA3 region of the rat hippocampus. The accumulation of nitrite, the stable metabolite of NO, was measured by the Griess reaction at different times (5 min, 15 min, 2 h, 48 h, and 7 days) in hippocampus, forebrain cortex, striatum, and cerebellum homogenates. The used glutamate antagonists APV and CNQX both provided sufficient neuroprotection in the sense of reducing nitrite concentrations, but with different mechanisms and time dynamics. Our findings suggest that NMDA and AMPA/kainate receptors are differentially involved in nitric oxide production.
Use of confocal microscopy in the study of ischemia-induced hippocampal neuronal damage
RadenoviLidija,Selakovi? Vesna,Baji? A.,Andjus P.R.
Archives of Biological Sciences , 2008, DOI: 10.2298/abs0804561r
Abstract: The present study was undertaken to reveal by means of confocal laser microscopy the cytoarchitecture of hippocampal CA3 neurons in Mongolian gerbils before and after cerebral ischemia of different duration. The common carotid arteries of gerbils were occluded for 5, 10, or 15 min. On the 4th, 14th and 28th day after reperfusion, neuronal damage was examined by laser scanning confocal microscopy in the CA3 region of hippocampus (30 μm slices). Slices were stained with fluorescent Nissl staining and fluorescent membrane tracer DiI. Increased duration of cerebral ischemia resulted in a progressive loss of hippocampal CA3 neurons. Four days after the ischemic insult, neuronal damage in the hippocampal CA3 region was mild but visible. On the 28th day after reperfusion, neuronal damage in the observed brain structure was most severe. These results demonstrate the temporal profile of neuronal damage after an ischemic insult as observed using confocal microscopy.
Nitric oxide production in the rat brain after kainate-induced seizure
RadenoviLidija Lj.,Jovanovi? Marina D.,Vasiljevi? Ivana D.,Ninkovi? Milica
Acta Veterinaria , 2002, DOI: 10.2298/avb0206319r
Abstract: We investigated the role of nitric oxide (NO) as a new neurotransmitter in the control of excitability and neurotoxicity of the hippocampus, forebrain cortex, striatum and cerebellum of the rat, as well as the possible functional interaction between NO and the glutamate system. Kainic acid is an endogenous excitotoxin acting on glutamate non-N-methyl-D-aspartate (non-NMDA) receptors, that leads to neurotoxic damage resembling the alterations observed in some neurological disorders. Stimulation of glutamate receptors induces neuronal NO release, which in turn modulates glutamate transmission. We also investigated the effects of 7-nitroindazole (7-NI), a selective neuronal nitric oxide synthase inhibitor in vivo, on nitrite concentration after kainic acid injection (0.5 mg/ml, pH 7.2) unilaterally into the CA3 region of the rat hippocampus. The accumulation of nitrite, the stable metabolite of NO, was measured by the Griess reaction at different times (5 min, 15 min, 2 h, 48 hand 7 days) following kainate injection in the ipsi- and contralateral hippocampus, forebrain cortex striatum and cerebellum homogenates. 7-NI (WOmicroM) can effectively inhibit NO synthesis in rat brain after kainate-induced intrahippocampal neurotoxicity, suppressed nitrite accumulation and attenuated neuronal damage induced by NMDA overactivity. All data showed that reduction of nitrite levels in the nervous system causes overactivity resulting from the absence of the NO-mediated modulatory action. The relatively transient nitric oxide synthase inhibitory effect of 7-NI following intracerebral injection should be taken into account when using this drug to evaluate the central effects of NO. The present results implicate neuronal NO generation in the pathogenesis of both direct and secondary excitotoxic neuronal injuries in vivo. As such they suggest that neuronal NO synthase inhibitors may be useful in the treatment of neurological diseases in which excitotoxic mechanisms play a role.
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