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Neuroprotectionby MK-801 following cerebral ischemia in Mongolian gerbils
Radenovi? Lidija,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.
Dopaminergic neurotransmission triggers ischemia-induced hyperactivity in Mongolian gerbils.
Yamamoto T,Araki H,Futagami K,Kawasaki H
Acta Medica Okayama , 2001,
Abstract: It is recognized that sustained ischemia-induced hyperactivity is related to abnormalities in dopamine function. However, it is unclear that dopaminergic neurotransmission triggers such ischemia-induced hyperactivity. Therefore, the relationship between dopaminergic neurotransmission and ischemia-induced hyperactivity was investigated in an animal model using Mongolian gerbils. When haloperidol 2 mg/kg was administered i.p. 30 min after ischemia, the ischemia-induced hyperactivity at 24 h after ischemia was blocked. General behavior was similar to that of sham-operated animals. Haloperidol at doses of 0.1 and 0.2 mg/kg had no effect on locomotor activity in sham-operated animals and decreased ischemia-induced hyperactivity when the drug was administered 24 h after ischemia; these doses did not have any effect on ischemia-induced hyperactivity when the drug was administered 30 min after ischemia. On the other hand, when the animal was confined to a small, restrictive cage for the 24 h period immediately following ischemic injury, locomotor activity at 24 h after ischemia increased. Such behavior also increased in animals when they were returned to their original more permissive cages immediately after ischemia. It is conceivable that the decrease in the level of activity was not related to ischemia-induced hyperactivity. These data suggested that the inhibition of ischemia-induced hyperactivity can be induced by complete blockage of dopaminergic receptors immediately after ischemia.
Preconditioning with L-alanyl-L-glutamine in a Mongolian Gerbil model of acute cerebral ischemia/reperfusion injury
Pires, Vilma Leite de Sousa;Souza, José Reniclebson Feitosa de;Guimar?es, Sergio Botelho;Silva Filho, Antonio Ribeiro da;Garcia, José Huygens Parente;Vasconcelos, Paulo Roberto Leit?o de;
Acta Cirurgica Brasileira , 2011, DOI: 10.1590/S0102-86502011000700004
Abstract: purpose: to investigate the effect of l-alanyl-l-glutamine (l-ala-gln) preconditioning in an acute cerebral ischemia/reperfusion (i/r) model in gerbils. methods: thirty-six mongolian gerbils (meriones unguiculatus), (60-100g), were randomized in 2 groups (n=18) and preconditioned with saline 2.0 ml (group-s) or 0.75g/kg of l-ala-gln, (group-g) administered into the femoral vein 30 minutes prior to i/r. each group was divided into three subgroups (n=6). anesthetized animals (urethane, 1.5g/kg, i.p.) were submitted to bilateral occlusion of common carotid arteries during 15 minutes. samples (brain tissue and arterial blood) were collected at the end of ischemia (t0) and after 30 (t30) and 60 minutes (t60) for glucose, lactate, myeloperoxidase (mpo), thiobarbituric acid reactive substances (tbars), glutathione (gsh) assays and histopathological evaluation. results: glucose and lactate levels were not different in studied groups. however glycemia increased significantly in saline groups at the end of the reperfusion period. tbars levels were significantly different, comparing treated (group-g) and control group after 30 minutes of reperfusion (p<0.05) in cerebral tissue. pretreatment with l-ala-gln promoted a significant increase in cerebral gsh contents in group-g at t30 (p<0.001) time-point compared with group-s. at t30 and t60, increased levels of gsh occurred in both time-points. there were no group differences regarding mpo levels. pyknosis, presence of red neurons and intracellular edema were significantly smaller in group-g. conclusion: preconditioning with l-ala-gln in gerbils submitted to cerebral ischemia/reperfusion reduces oxidative stress and degeneration of the nucleus (pyknosis) and cell death (red neurons) in the cerebral tissue.
Effect of L-Deprenyl on the Putrescine Level and Neuronal Damage after Transient Global Cerebral Ischemia in Gerbils  [PDF]
Hyung Lee, Yeun-Kyung Chu, Joon-Ho Shon, Kyung-Hee Chun, Jee-In Kim, Seong-Ryong Lee
International Journal of Organic Chemistry (IJOC) , 2017, DOI: 10.4236/ijoc.2017.72014
Abstract: L-Deprenyl is selective and irreversible monoamine oxidase B inhibitor, known to have neuroprotective properties. Putrescine, one of polyamine, is thought to be important in the neuronal cell damage associated with various type of excitatory neurotoxicity. We examined the effects of L-deprenyl on the changes in putrescine level and neuronal damage after transient global ischemia in ger-bils. Male Mongolian gerbils weighing 65 - 75 g were used in the experiment. Global ischemia was induced by occlusion of common carotid arteries for 3 min to observe neuronal injury in hippocampal pyramidal cells. L-Deprenyl group was given 10 mg/kg of L-deprenyl intraperitoneally immediately after, 3 h and 6 h after global ischemia. Treated animals were processed in parallel with ischemic animals receiving saline as a vehicle and with sham- operated controls. Hippocampal putrescine level was increased by global ischemia and inhibited by L-deprenyl treatment. In histological findings, counts of viable neurons were made in the pyramidal cell layer of the hippocampal CA1 area 3 days after ischemic insult. The number of viable neurons in the pyramidal cell layer of CA1 area was significantly increased in animals treated with L-deprenyl compared to vehicle-treated ischemic animals (p < 0.05). In terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick endlabeling (TUNEL) assay, semiquantitative analysis of dark-brown neuronal cells was made in the hippocampal CA1 area. There was also a significant difference in the degree of TUNEL staining in the hippocampal CA1 area between vehi-cle-treated and L-deprenyl-treated animals (p < 0.05). These data show L-deprenyl is effective as a prophylactic treatment for neuronal injury when it is administrated before ischemia but a further study need to know the effects of administration of L-deprenyl after ischemia and at given times after reper-fusion.
Determination of interhemispheric neuroprotective action of the cognitive enhancer Phenibute at an experimental ischemic stroke in Gerbils  [PDF]
Mamchur V.I.,Zhuravel’ N.V.
Морфолог?я , 2008,
Abstract: In experiments on Mongolian gerbils the study of neuroprotective properties of the cognitive enhancer Phenibute was conducted. Pathology was studied on the generally accepted model for this type of laboratory animals taking into account the features of the cerebral blood circulation (ischemia and reperfusion). The influence of preparation was explored on the terms of regress of neurological deficit in gerbils with the hemispheric localization of ischemic strokes. A neuromorphological study is conducted influence of nootrop on renewal of nervous fabric in the early terms of ischemia. On the 4th days of ischemia the morphological and functional condition of neurons and maintenance of РNA in them was studied. Some interhemispheric influencing distinctions of Phenibute on renewal of neurons of bark right and left hemispheres were sited. A tendency is exposed to more effective renewals of nervous fabric of right hemisphere under influencing of Phenibute at pres-ence of symmetric hearths of cerebral infarct. Findings can be used for development of rational charts of treatment of pathol-ogy of brain with hemispheric localization.
Extremely Low Frequency Magnetic Field (50 Hz, 0.5 mT) Reduces Oxidative Stress in the Brain of Gerbils Submitted to Global Cerebral Ischemia  [PDF]
Sne?ana Rau? Balind, Vesna Selakovi?, Lidija Radenovi?, Zlatko Proli?, Branka Jana?
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0088921
Abstract: Magnetic field as ecological factor has influence on all living beings. The aim of this study was to determine if extremely low frequency magnetic field (ELF-MF, 50 Hz, 0.5 mT) affects oxidative stress in the brain of gerbils submitted to 10-min global cerebral ischemia. After occlusion of both carotid arteries, 3-month-old gerbils were continuously exposed to ELF-MF for 7 days. Nitric oxide and superoxide anion production, superoxide dismutase activity and index of lipid peroxidation were examined in the forebrain cortex, striatum and hippocampus on the 7th (immediate effect of ELF-MF) and 14th day after reperfusion (delayed effect of ELF-MF). Ischemia per se increased oxidative stress in the brain on the 7th and 14th day after reperfusion. ELF-MF also increased oxidative stress, but to a greater extent than ischemia, only immediately after cessation of exposure. Ischemic gerbils exposed to ELF-MF had increased oxidative stress parameters on the 7th day after reperfusion, but to a lesser extent than ischemic or ELF-MF-exposed animals. On the 14th day after reperfusion, oxidative stress parameters in the brain of these gerbils were mostly at the control levels. Applied ELF-MF decreases oxidative stress induced by global cerebral ischemia and thereby reduces possible negative consequences which free radical species could have in the brain. The results presented here indicate a beneficial effect of ELF-MF (50 Hz, 0.5 mT) in the model of global cerebral ischemia.
The protective effect of M40401, a superoxide dismutase mimetic, on post-ischemic brain damage in Mongolian gerbils  [cached]
Mollace Vincenzo,Iannone Michelangelo,Muscoli Carolina,Palma Ernesto
BMC Pharmacology , 2003, DOI: 10.1186/1471-2210-3-8
Abstract: Background Overproduction of free radical species has been shown to occur in brain tissues after ischemia-reperfusion injury. However, most of free radical scavengers known to antagonize oxidative damage (e.g. superoxide dismutase, catalase), are unable to protect against ischemia-reperfusion brain injury when given in vivo, an effect mainly due to their difficulty to gain access to brain tissues. Here we studied the effect of a low molecular weight superoxide dismutase mimetic (M40401) in brain damage subsequent to ischemia-reperfusion injury in Mongolian gerbils. Results In animals undergoing ischemia-reperfusion injury, neuropathological and ultrastructural changes were monitored for 1–7 days either in the presence or in the absence of M40401 after bilateral common carotid artery occlusion (BCCO). Administration of M40401 (1–40 mg/kg, given i.p. 1 h after BCCO) protected against post-ischemic, ultrastructural and neuropathological changes occurring within the hippocampal CA1 area. The protective effect of M40401 was associated with a significant reduction of the levels of malondialdehyde (MDA; a marker of lipid peroxidation) in ischemic brain tissues after ischemia-reperfusion. Conclusion Taken together, these results demonstrate that M40401 provides protective effects when given early after the induction of ischemia-reperfusion of brain tissues and suggest the possible use of such compounds in the treatment of neurological dysfunction subsequent to cerebral flow disturbances.
Time course of oxidative damage in different brain regions following transient cerebral ischemia in gerbils  [PDF]
E. Candelario-Jalil,N. H. Mhadu,S. M. Al-Dalain,G. Martinez,O. S. Leon
Quantitative Biology , 2007,
Abstract: The time course of oxidative damage in different brain regions was investigated in the gerbil model of transient cerebral ischemia. Animals were subjected to both common carotid arteries occlusion for 5 min. After the end of ischemia and at different reperfusion times (2, 6, 12, 24, 48, 72, 96 h and 7 days), markers of lipid peroxidation, reduced and oxidized glutathione levels, glutathione peroxidase, glutathione reductase, manganese-dependent superoxide dismutase (MnSOD) and copper/zinc containing SOD (Cu/ZnSOD) activities were measured in hippocampus, cortex and striatum. Oxidative damage in hippocampus was maximal at late stages after ischemia (48-96 h) coincident with a significant impairment in glutathione homeostasis. MnSOD increased in hippocampus at 24, 48 and 72 h after ischemia, coincident with the marked reduction in the activity of glutathione-related enzymes. The late disturbance in oxidant-antioxidant balance corresponds with the time course of delayed neuronal loss in the hippocampal CA1 sector. Cerebral cortex showed early changes in oxidative damage with no significant impairment in antioxidant capacity. Striatal lipid peroxidation significantly increased as early as 2 h after ischemia and persisted until 48 h with respect to the sham-operated group. These results contribute significant information on the timing and factors that influence free radical formation following ischemic brain injury, an essential step in determining effective antioxidant intervention.
The highly selective cyclooxygenase-2 inhibitor DFU is neuroprotective when given several hours after transient cerebral ischemia in gerbils  [PDF]
E. Candelario-Jalil,D. Alvarez,J. M. Castaneda,S. M. Al-Dalain,G. Martinez-Sanchez,N. Merino,O. S. Leon
Quantitative Biology , 2007,
Abstract: Several studies suggest that cyclooxygenase-2 contributes to the delayed progression of ischemic brain damage. In this study we examined whether the highly selective cyclooxygenase-2 inhibitor DFU reduces neuronal damage when administered several hours after 5 min of transient forebrain ischemia in gerbils. The extent of ischemic injury was assessed behaviorally by measuring the increases in locomotor activity and by histopathological evaluation of the extent of CA1 hippocampal pyramidal cell injury 7 days after ischemia. DFU treatment (10 mg/kg, p.o.) significantly reduced hippocampal neuronal damage even if the treatment is delayed until 12 h after ischemia. These results suggest that selective cyclooxygenase-2 inhibitors may be a valuable therapeutic strategy for ischemic brain injury.
Use of confocal microscopy in the study of ischemia-induced hippocampal neuronal damage  [PDF]
Radenovi? Lidija,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.
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