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Delayed neuronal cell death in brainstem after transient brainstem ischemia in gerbils
Fang Cao, Ryuji Hata, Pengxiang Zhu, Shoichiro Takeda, Tadashi Yoshida, Nobuhiro Hakuba, Masahiro Sakanaka, Kiyofumi Gyo
BMC Neuroscience , 2010, DOI: 10.1186/1471-2202-11-115
Abstract: Brainstem ischemia was produced by occlusion of the bilateral vertebral arteries just before their entry into the transverse foramina of the cervical vertebrae of Mongolian gerbils. Animals were subjected to brainstem ischemia for 15 min, and then reperfused for 0 d (just after ischemia), 1 d, 3 d and 7 d (n = 4 in each group). Sham-operated animals (n = 4) were used as control. After deep anesthesia, the gerbils were perfused with fixative for immunohistochemical investigation. Ischemic lesions were detected by immunostaining for microtubule-associated protein 2 (MAP2). Just after 15-min brainstem ischemia, ischemic lesions were detected in the lateral vestibular nucleus and the ventral part of the spinal trigeminal nucleus, and these ischemic lesions disappeared one day after reperfusion in all animals examined. However, 3 days and 7 days after reperfusion, ischemic lesions appeared again and clusters of ionized calcium-binding adapter molecule-1(IBA-1)-positive cells were detected in the same areas in all animals.These results suggest that delayed neuronal cell death took place in the brainstem after transient brainstem ischemia in gerbils.In the central nervous system, certain areas are selectively damaged even after a brief ischemic insult, and this topographical heterogeneity is known as "selective vulnerability of the brain". Hippocampal CA1 and neocortical III, V, and VI are extremely vulnerable to ischemia and hypoxia [1]. The mechanism responsible for this vulnerability is of particular importance to establish therapeutic procedures, because elucidation of the mechanism may lead to the development of novel therapy to ameliorate ischemic damage.Pathologic aspects and the topographic distribution of ischemic lesions after transient ischemia have been extensively studied in the rodent forebrain [2,3]. However, little is known about the distribution of ischemic lesions after transient brainstem ischemia because of the lack of reproducible brainstem ischemia mo
Effect of policosanol on cerebral ischemia in Mongolian gerbils  [cached]
Molina V.,Arruzazabala M.L.,Carbajal D.,Valdés S.
Brazilian Journal of Medical and Biological Research , 1999,
Abstract: Policosanol is a mixture of higher aliphatic primary alcohols isolated from sugar cane wax, whose main component is octacosanol. An inhibitory effect of policosanol on platelet aggregation and cerebral ischemia in animal models has been reported. Thus, the objective of the present study was to evaluate the effect of policosanol on cerebral ischemia induced by unilateral carotid ligation and bilateral clamping and recirculation in Mongolian gerbils. Policosanol (200 mg/kg) administered immediately after unilateral carotid ligation and at 12- or 24-h intervals for 48 h significantly inhibited mortality and clinical symptoms when compared with controls, whereas lower doses (100 mg/kg) were not effective. Control animals showed swelling (tissue vacuolization) and necrosis of neurons in all areas of the brain studied (frontal cortex, hippocampus, striatum and olfactory tubercle), showing a similar injury profile. In the group treated with 200 mg/kg policosanol swelling and necrosis were significantly reduced when compared with the control group. In another experimental model, comparison between groups showed that the brain water content of control gerbils (N = 15) was significantly higher after 15 min of clamping and 4 h of recirculation than in sham-operated animals (N = 13), whereas policosanol (200 mg/kg) (N = 19) significantly reduced the edema compared with the control group, with a cerebral water content identical to that of the sham-operated animals. cAMP levels in the brain of control-ligated Mongolian gerbils (N = 8) were significantly lower than those of sham-operated animals (N = 10). The policosanol-treated group (N = 10) showed significantly higher cAMP levels (2.68 pmol/g of tissue) than the positive control (1.91 pmol/g of tissue) and similar to those of non-ligated gerbils (2.97 pmol/g of tissue). In conclusion, our results show an anti-ischemic effect of policosanol administered after induction of cerebral ischemia, in two different experimental models in Mongolian gerbils, suggesting a possible therapeutic effect in cerebral vascular disorders.
Effect of policosanol on cerebral ischemia in Mongolian gerbils
Molina, V.;Arruzazabala, M.L.;Carbajal, D.;Valdés, S.;Noa, M.;Más, R.;Fraga, V.;Menéndez, R.;
Brazilian Journal of Medical and Biological Research , 1999, DOI: 10.1590/S0100-879X1999001000014
Abstract: policosanol is a mixture of higher aliphatic primary alcohols isolated from sugar cane wax, whose main component is octacosanol. an inhibitory effect of policosanol on platelet aggregation and cerebral ischemia in animal models has been reported. thus, the objective of the present study was to evaluate the effect of policosanol on cerebral ischemia induced by unilateral carotid ligation and bilateral clamping and recirculation in mongolian gerbils. policosanol (200 mg/kg) administered immediately after unilateral carotid ligation and at 12- or 24-h intervals for 48 h significantly inhibited mortality and clinical symptoms when compared with controls, whereas lower doses (100 mg/kg) were not effective. control animals showed swelling (tissue vacuolization) and necrosis of neurons in all areas of the brain studied (frontal cortex, hippocampus, striatum and olfactory tubercle), showing a similar injury profile. in the group treated with 200 mg/kg policosanol swelling and necrosis were significantly reduced when compared with the control group. in another experimental model, comparison between groups showed that the brain water content of control gerbils (n = 15) was significantly higher after 15 min of clamping and 4 h of recirculation than in sham-operated animals (n = 13), whereas policosanol (200 mg/kg) (n = 19) significantly reduced the edema compared with the control group, with a cerebral water content identical to that of the sham-operated animals. camp levels in the brain of control-ligated mongolian gerbils (n = 8) were significantly lower than those of sham-operated animals (n = 10). the policosanol-treated group (n = 10) showed significantly higher camp levels (2.68 pmol/g of tissue) than the positive control (1.91 pmol/g of tissue) and similar to those of non-ligated gerbils (2.97 pmol/g of tissue). in conclusion, our results show an anti-ischemic effect of policosanol administered after induction of cerebral ischemia, in two different experimental models i
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.
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.
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.
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.
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.
Neuroprotective efficacy of nimesulide against hippocampal neuronal damage following transient forebrain ischemia  [PDF]
E. Candelario-Jalil,D. Alvarez,A. Gonzalez-Falcon,M. Garcia-Cabrera,G. Martinez-Sanchez,N. Merino,A. Giuliani,O. S. Leon
Quantitative Biology , 2007,
Abstract: Cyclooxygenase-2 is involved in the inflammatory component of the ischemic cascade, playing an important role in the delayed progression of the brain damage. The present study evaluated the pharmacological effects of the selective cyclooxygenase-2 inhibitor nimesulide on delayed neuronal death of hippocampal CA1 neurons following transient global cerebral ischemia in gerbils. Administration of therapeutically relevant doses of nimesulide (3, 6 and 12 mg/kg; i.p.) 30 min before ischemia and at 6, 12, 24, 48 and 72 h after ischemia significantly (P<0.01) reduced hippocampal neuronal damage. Treatment with a single dose of nimesulide given 30 min before ischemia also resulted in a significant increase in the number of healthy neurons in the hippocampal CA1 sector 7 days after ischemia. Of interest is the finding that nimesulide rescued CA1 pyramidal neurons from ischemic death even when treatment was delayed until 24 h after ischemia (34+/-9% protection). Neuroprotective effect of nimesulide is still evident 30 days after the ischemic episode, providing the first experimental evidence that cyclooxygenase-2 inhibitors confer a long-lasting neuroprotection. Oral administration of nimesulide was also able to significantly reduce brain damage, suggesting that protective effects are independent of the route of administration. The present study confirms the ability of cyclooxygenase-2 inhibitors to reduce brain damage induced by cerebral ischemia and indicates that nimesulide can provide protection when administered for up to 24 h post-ischemia.
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.
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