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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Mongolian gerbils, bilateral carotid occlusion (BCO) followed by reperfusion causes uniform destruction of the CA1 pyramidal neurons in the hippocampus, and this damage correlates with an increase in locomotor activity. Various drugs, such as NMDA antagonists, calcium channel blockers, and free radical scavengers, have provided neuroprotection against ischaemia-induced damage. More recently, the neuroprotective effects of dopamine have been investigated. A large release of dopamine has been shown to occur at the onset of ischaemia, and dopamine levels return to basal values following reperfusion. In the present study, we investigated the effects of vanoxeamine (GBR 12909) (5 or 10 mg/kg i.p., administered 1 h prior to occlusion) on behavioural and histological changes following global ischaemia in the Mongolian gerbil. Ischaemia was induced by bilateral carotid occlusion for 5 min. Both doses of GBR 12909 significantly potientiated the hyperactivity of the BCO animals measured in the home cage during the first 24 h following surgery and in the locomotor activity arena after 24 h and 48 h. Significant neuroprotection of cells in the CA1 region of the bippocampus was observed in drug-treated animals 96 h postsurgery. The neuroprotective effect of GBR 12909 may be ascribed to sensitisation of the dopamine D, autoreceptor, consequently reducing the release of dopamine that occurs following ischaemia. Alternatively, GBR 12909 may have a direct interaction with the Na+ ion channel-glutamate complex, resulting in reduced release of glutamate and thereby reducing NMDA receptor activation and neuronal damage.
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PMID:Protective effects of vanoxeamine (GBR 12909) against ischaemia-induced hyperactivity and neurodegeneration in the gerbil model of cerebral ischaemia. 913 Mar

Five minutes of global ischemia in gerbil results in delayed hippocampal CA1 neuronal degeneration, which is accompanied by working memory impairments and hyperactivity in novel environments. In this study, postischemic activity was characterized in familiar and in novel environments to determine whether hyperactivity was due to impaired spatial habituation or another form of motor hyperactivity. This study also determined whether 6-h delayed hypothermia, which reduces CA1 neuronal injury, would attenuate functional impairments. Gerbils were subjected to 5 min of normothermic ischemia or sham operation 2 days following implantation of brain temperature probes. One of two ischemic groups was cooled (>48 h) starting at 6-h postischemia. Locomotor activity in a familiar cage was measured for 6 days while activity in three novel environments was intermittently measured on days 4, 5 and 6. Open field behavior and working memory in a T-maze were also assessed. Untreated ischemia caused marked hyperactivity in the familiar cage on day 1, which reverted to near-normal by day 2. Nonetheless, these gerbils showed hyperactivity during novel environment sessions on days 4-6. This maze behavior, which predicted hippocampal CA1 injury, was not due to different habituation rates nor baseline hyperactivity. Conversely, open field sessions on day 8 revealed ischemic habituation rate deficits. Ischemia also impaired working memory in the T-maze. Delayed hypothermia, which reduced neuronal loss in the CA1 sector to 12% from 81%, reduced all functional impairments. Ischemic gerbils quickly developed spontaneous locomotion hyperactivity that returned to near-normal after 1 day. This motor hyperactivity did not explain the elevated activity found with delayed testing in novel environments. Regardless, only the open field test on day 8 revealed a habituation-like deficit.
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PMID:Characterization of postischemic behavioral deficits in gerbils with and without hypothermic neuroprotection. 972 85

Biotelemetry is a new biological technology which evaluates continuous spontaneous locomotor activity and body temperature in rodents. The telemetry system comprises a transmitter implanted in the peritoneal cavity of the rodent, and a receiver placed beneath the animal's cage. The receiver detects the radio waves and the activity of the rodents as counts which are registered in the computer system, and the adapter detects the calibrated body temperature. First, we showed that biotelemetric studies of different species (rats, guinea pigs, mice and gerbils) provide substantial information about their circadian rhythms. Second, using the most common examples employed in pharmacology of inflammation (hyperthermia, arthritis, ischemia-reperfusion and so on) biotelemetry has helped us to clarify the pathophysiological significance of the parameters of temperature and mobility in several experimental models in rodents.
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PMID:Biotelemetry: an original approach to experimental models of inflammation. 1049 58

We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels ( approximately 106 +/- 4 microm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was approximately 25, 40, and 60% of KCl-induced preconstriction after the long-term, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside-evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by approximately 70 and approximately 160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.
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PMID:Microvascular and myocardial contractile responses to ischemia: influence of exercise training. 1065 8

We investigated the brain protection effects of propofol anesthesia and nitrous oxide-oxygen-isoflurane anesthesia (GOI) using forebrain ischemic model of male Sprague-Dawley rats. Propofol group (P, n = 15) was anesthetized with propofol, oxygen and nitrogen (FIO2 = 0.33), and isoflurane group (GOI, n = 15) with 66% nitrous oxide, 33% oxygen and 1.2% isoflurane under mechanical ventilation. The anesthesia was deepened until electroencephalographic burst suppression appeared in each group. The bilateral common carotid arteries were, then, occluded for 10 minutes while the blood pressure was maintained at about 40 mmHg by venesection. The venesected blood was returned at the end of ischemic period. The animals were kept and fed in cage after emergence. On the day 2, 4, and 7, five animals of each group were sacrificed and the microscopic samples were obtained. The CA-1 cells of hippocampus were then stained with hematoxylin and eosin for the delayed neuronal death (DND) and with TUNEL method for the apoptosis. Propofol reduced the apoptosis, i.e., reduced the TUNEL positive cell count (GOI = 121.2 +/- 25.2.mm-1; P = 53.8 +/- 11.4.mm-1; P < 0.01; mean +/- SD) on the day 2 after ischemia, and also reduced the delayed neuronal death (alive CA-1 cell count; GOI = 18.1 +/- 8.9.mm-1; P = 33.1 +/- 12.8.mm-1; P < 0.01) on the day 7 after ischemia. It is important to determine the recovery interval after brain ischemia in detection of DND and apoptosis. We conclude that propofol inhibits neuronal apoptosis after brain ischemia and consequently reduces the delayed neuronal death in the CA-1 pyramidal cell layer of the hippocampus.
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PMID:[Depressive effects of propofol on apoptotic injury and delayed neuronal death after forebrain ischemia in the rat--comparison with nitrous oxide-oxygen-isoflurane]. 1070 15

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.
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PMID:Dopaminergic neurotransmission triggers ischemia-induced hyperactivity in Mongolian gerbils. 1168 50

This study addresses the effects of induced hyperthermia on post-ischemic rat brain evaluated histologically and/or immunohistochemically after 7-day, 2-month or 6-month survival. Hyperthermia (38.5 degrees - 40 degrees C) maintained (by heating the cage environment to 34-35 degrees C) for two consecutive periods of 5 and 9 h timed, respectively, from 4- and 21-h recirculation following 10-min global ischemia (two-vessel occlusion + hypotension) induced chronic neuronal death that became apparent in the rat forebrain from 7-day to 2-month survival. Associated immunohistochemical findings after 2 or 6 months of recovery included: (1) complement activation (membrane attack complex formation); (2) generalized overexpression of ubiquitin in surviving forebrain neurons; (3) persistent activation of macrophages; (4) presence of gemistocytic astrocytes in the hippocampus; (5) maturation of amyloid plaques (identified by immunohistochemistry using anti-human beta-A4 primary antibody) in cerebral cortex; and (6) intracellular deposits identified by anti-human hyperphosphorylated tau protein antibodies. This novel non-transgenic, self-sustained model of neurodegeneration triggered by the association of two prevalent insults to the aging human brain (ischemia and hyperthermia) presents morphological features similar to those of Alzheimer's disease. This finding raises the possibility that febrile complications of acute brain injuries may similarly impair human cognitive function in the long run.
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PMID:Postischemic hyperthermia induces Alzheimer-like pathology in the rat brain. 1193 59

Acute mitral regurgitation (MR) is present in 10% of patients presenting with cardiogenic shock. To stabilize these patients, intra-aortic balloon pumping (IABP) is recommended, but the mechanism of IABP support in these patients is unknown. This animal study was designed to describe the hemodynamic effect of intra-aortic balloon pumping during cardiogenic shock induced by acute MR. In eight calves, left ventricular pressure-volume loops, aortic and left atrial pressure, and aortic, carotid artery, and coronary blood flow were recorded. Acute MR (range 36%-79%) was created by placing a metal cage in the mitral valve. Hemodynamic data was obtained at control, during acute MR, and during acute MR with 1:1 IABP support. Acute MR caused a decrease in cardiac output (-32%, P = 0.018), blood pressure, and carotid artery flow, whereas left ventricular output (+127%, P = 0.018), end-diastolic volume, and left atrial pressure all significantly increased. Stroke work, ejection fraction, and coronary blood flow were not significantly changed, and no signs of ischemia were seen on the ECG. The IABP raised average cardiac output by 31% (P = 0.012) and significantly raised blood pressure and flow to the brain while decreasing systemic vascular resistance. Left ventricular function and mean coronary blood flow did not change, but diastolic coronary flow became more important as shown by the increase in diastolic fraction from 64% to 95%. (P = 0.028). Average MR dropped by 7.5% (P = 0.025). In conclusion, application of the IABP during acute MR lowers aortic impedance, resulting in less MR and more output toward the aorta without changing left ventricular function.
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PMID:Intra-aortic balloon pumping in acute mitral regurgitation reduces aortic impedance and regurgitant fraction. 1268 44

Housing rats in an enriched environment improves functional outcome after ischemic stroke, this may reflect neuronal plasticity in brain regions outside the lesion. Which components of the enriched environment that are of greatest importance for recovery after brain ischemia is uncertain. We have previously found that enriched environment and social interaction alone both improve functional recovery after focal cerebral ischemia, compared with isolated housing with voluntary wheel-running. In this study, the aim was to separate components of the enriched environment and investigate the effects on some potential mediators of improved functional recovery; such as the inducible transcription factors nerve growth factor-induced gene A (NGFI-A) and NGFI-B, and the glucocorticoid and serotonin systems. After permanent middle cerebral artery occlusion, rats were divided into four groups: individually housed with no equipment (deprived group), individually housed with free access to a running wheel (running group), housed together in a large cage with no equipment (social group) or in a large cage furnished with exchangeable bars, chains and other objects (enriched group). mRNA expression of inducible transcription factors, serotonin and glucocorticoid receptors was determined with in situ hybridisation 1 month after cerebral ischemia. Rats housed in enriched or social environments showed significantly higher mRNA expression of NGFI-A and NGFI-B in cortical regions outside the lesion and in the CA1 (cornu ammonis region of the hippocampus), compared with isolated rats with or without a running wheel. NGFI-A and NGFI-B mRNA expression in cortex and in CA1 was significantly correlated to functional outcome. 5-Hydroxytryptamine receptor 1A (5-HT(1A)) mRNA expression and binding, as well as 5-HT(2A) receptor mRNA expression were decreased in the hippocampus (CA4 region) of the running wheel rats. Mineralocorticoid receptor gene expression was increased in the dentate gyrus amongst wheel-running rats. No group differences were found in plasma corticosterone levels or mRNA levels of glucocorticoid receptor, corticotropin-releasing hormone, 5-HT(2C) or c-fos. In conclusion, we have found that social interaction is a major component of the enriched environment regarding the effects on NGFI-A and NGFI-B expression. These transcription factors may be important mediators of improved functional recovery after brain infarctions, induced by environmental enrichment.
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PMID:Effects of postischemic environment on transcription factor and serotonin receptor expression after permanent focal cortical ischemia in rats. 1280 85

NGP1-01, a member of the pentacycloundecylamine cage compound family, was recently shown to exhibit both NMDA receptor channel blocking and L-type calcium channel antagonism activity. In the present study, focal ischemia was induced in mice by permanent middle cerebral artery occlusion (MCAO) to test for potential neuroprotective properties of the compound. In female CD-1 mice injected 30 min before MCAO, NGP1-01 (20 mg/kg) reduced infarct area by 42.6% (P < 0.05) compared to vehicle-treated controls as visualized by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Concomitantly, NGP1-01 reduced brain swelling by 78.3% (P < 0.001), compared to vehicle (DMSO) treated controls. These data identify NGP1-01 and related compounds as potential lead structures to develop neuroprotective compounds based on a dual mechanism of action.
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PMID:NGP1-01, a lipophilic polycyclic cage amine, is neuroprotective in focal ischemia. 1593 10


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