Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Social olfactory recognition in rodents has been shown to assess short-term memory and to be sensitive to cholinergic drugs. It is based on the investigation of a juvenile by an adult rat and is measured by a reduction in duration of exploration during the second of two successive exposures lasting 5min. The present experiments further characterize rodent social recognition in pathophysiological models known to impair memory. Social recognition was distrupted by ageing in both rats and mice, by vincristine-induced septal lesion and by damaging the CA1 hippocampal layer after cerebral ischaemia in rats. These memory deficits could be compensated by reducing the time interval between the two presentations of the juvenile and/or by prolonging the juvenile encounter. Similarly, muscarinic agonists (arecoline, SR 46559A) counterbalanced the memory impairment in the three models. The present results indicate that the hippocampus plays a key role in social recognition. They suggest that in the three pathophysiological models, memory ability is still present although it is of very short duration; however, it can still be improved by pharmacological treatments.
 ...
PMID:Social olfactory recognition in rodents: deterioration with age, cerebral ischaemia and septal lesion. 1122 55

The protective effect of hyperin (Hyp) against cerebral ischemia-reperfusion injury was studied. On the cerebral ischemia-reperfusion model in mice, Hyp (50, 100 mg.kg-1, i.p.) was shown to markedly and dose-dependently inhibit the decrease of lactate dehydrogenase (LDH) in cerebrum and improve the learning and memory impairment on the step down test. On the four-vessel occlusion model in rats, Hyp(50 and 100 mg.kg-1, i.p.) significantly reduced the decreases of glutathione peroxidase(GSH-Px), superoxide dismutase(SOD) and LDH activities in the cerebrum. Hyp was also shown to inhibit the increase of nitric oxide (NO) and malondialdehyde (MDA) contents in the cerebrum and promote the recovery of EEG activities. These results suggest that Hyp has protective effect against cerebral ischemia-reperfusion injury via attenuating free radical and NO.
 ...
PMID:[Protective effect of hyperin against cerebral ischemia-reperfusion injury]. 1193 28

In the present study, we investigated the effects of N(G)-nitro-L-arginine (L-NAME), an inhibitor of nitric oxide synthase, on repeated cerebral ischemia-induced impairment of spatial memory of the 8-arm radial maze in rats. Repeated ischemia (10 min ischemia x 2 times with 1 h interval) impaired the spatial memory in the 8-arm radial maze test and produced apoptosis in the hippocampus 7 days after final occlusion, and gradually increased the NO(x)(-) levels approximately 30-180 min after the second reperfusion. Post-ischemic administration of L-NAME at a dose of 50 mg/kg, i.p. 30 min following the second occlusion, significantly attenuated the repeated ischemia-induced impairment of spatial memory in the 8-arm radial maze test and suppressed apoptosis in the hippocampus, and also significantly suppressed a delayed increase in the NO(x)(-) levels induced by repeated ischemia. However, pre-ischemic administration of L-NAME at a dose of 50 mg/kg, i.p. 30 min before the first occlusion, caused about 90% mortality (the mortality rate of vehicle-treated group was 10%). These results suggest that the delayed generation of NO(x)(-) may cause spatial memory impairment and induction of apoptosis in the hippocampus in rats subjected to repeated ischemia.
 ...
PMID:Post-ischemic administration [correction of administeration] but not pre-ischemic administration [correction of administeration] of NG-nitro-L-arginine prevents spatial memory impairments and apoptosis by an inhibition of a delayed increase in NOx- in the hippocampus following repeated cerebral ischemia. 1264 90

We investigated the effects of nilvadipine and amlodipine on the cerebral ischemia-induced impairment of spatial memory in 8-arm radial maze performance and hippocampal CA1 apoptosis in rats. Single cerebral ischemia impaired memory without inducing apoptosis. In these rats, neither nilvadipine nor amlodipine at 3.2 mg/kg, i.p. improved the impaired memory. On the other hand, repeated cerebral ischemia (10 min ischemia x 2, 1 h interval) impaired spatial memory and induced hippocampal apoptosis 7 days after the final occlusion/reperfusion. Moreover, repeated ischemia increased the apoptotic cell number, an effect observed after 3 days and peaked after 7 days. However, mRNA expression of the apoptosis-related early oncogene bax and CPP 32 (caspase-3) was observed after 24 h. In these rats, nilvadipine, but not amlodipine, significantly improved memory, concomitantly decreased hippocampal apoptosis, and suppressed both bax and CPP 32 expression. These results suggest that nilvadipine improved the memory impairment in repeated ischemia by reducing bax and CPP 32 expression and suppressing the induction of apoptosis in the hippocampus. Nilvadipine may have a neuroprotective effect and could be a useful pharmacotherapeutic agent for cerebrovascular dementia.
 ...
PMID:Effect of nilvadipine on the cerebral ischemia-induced impairment of spatial memory and hippocampal apoptosis in rats. 1457 87

In the present experiment, we studied the action of buckwheat polyphenol (BWP, from Fagopyrum esculentum MOENCH) in a repeated cerebral ischemia model, which induced a strong and long-lasting impairment of spatial memory in 8-arm radial maze with hippocampal CA1 cell death in rats. BWP (600 mg/kg, continuous 21-day p.o.) significantly ameliorated not only the impairment of spatial memory in the 8-arm radial maze, but also necrosis and TUNEL-positive cells in the hippocampal CA1 area subjected to repeated cerebral ischemia (10 min x 2 times occlusion, 1-h interval) in rats. In order to investigate the mechanism of BWP protective action, we measured the release of glutamate and NO(x)(-) (NO(2)(-) + NO(3)(-)) production induced by repeated cerebral ischemia in the rat dorsal hippocampus using microdialysis. A 14-day BWP treatment significantly inhibited the excess release of glutamate after the second occlusion. In addition, the BWP remarkably suppressed a delayed increase in NO(x)(-) (NO(2)(-) + NO(3)(-)) induced by repeated cerebral ischemia in the dorsal hippocampus as determined in vivo by microdialysis. However, the 14-day treatment did not affect hippocampal blood flow in either intact rats or rats subjected to repeated ischemia measured by lasser Doppler flowmeter. These results suggested that BWP might ameliorate spatial memory impairment by inhibiting glutamate release and the delayed generation of NO(x)(-) in rats subjected to repeated cerebral ischemia.
 ...
PMID:Protective effect of buckwheat polyphenols against long-lasting impairment of spatial memory associated with hippocampal neuronal damage in rats subjected to repeated cerebral ischemia. 1510 79

1. Capsaicin, the irritant principle of hot peppers, is a vanilloid agonist known to activate the transient receptor potential channel vanilloid subfamily member 1 (VR1), recently reported to be involved in neurodegeneration. The present study investigated the role of VR1 in a model of global cerebral ischemia in gerbils. 2. Over the dose range tested, capsaicin (0.01, 0.025, 0.05, 0.2 and 0.6 mg kg(-1)), given 5 min after recirculation, dose-dependently antagonized the ischemia-induced electroencephalographic total spectral power decrease and restored relative frequency band distribution evaluated 7 days after ischemia. 3. Capsaicin, at all tested doses, fully prevented ischemia-induced hyperlocomotion evaluated 1 day after ischemia. 4. Capsaicin dose-dependently antagonized ischemia-induced memory impairment evaluated in a passive avoidance task, 3 days after ischemia. 5. Capsaicin showed a dose-dependent hypothermic effect evaluated for 2 h after recirculation. 6. At 7 days after ischemia, a progressive survival of pyramidal cells in the CA1 subfield in capsaicin-treated gerbils, with a maximum of 80%, at a dose of 0.2 mg kg(-1), was obtained. 7. The selective VR1 antagonist, capsazepine (0.01 mg kg(-1)), reversed capsaicin-induced protective effects, in a competitive manner. 8. These results suggest that the neuroprotective effect of capsaicin may be attributable, at least in part, to VR1 desensitization and provide a valuable target for development of interventional pharmacological strategies.
 ...
PMID:Capsaicin exhibits neuroprotective effects in a model of transient global cerebral ischemia in Mongolian gerbils. 1567 80

Frequency of clinical and psychological peculiarities of moderate (mild) cognitive impairment (MCI) in cerebral vascular insufficiency (CVI) was studied in 42 patients, mean age 67.7 +/- 7.7 years. Along with neurological examination, a battery of psychiatric and neuropsychological scales and tests was used. MCI was diagnosed in 28 (66.7%) patients. In 20 patients (47.6%), cognitive hypoactivity was most prominent related to impaired neurodynamics and regulation of voluntary activity which may reflect subcortical and frontal lobes functions. In 8 patients (20.1%), there was a prominent memory impairment characteristic of hippocampus lesion. The authors suggest the presence of concomitant neurodegeneration in patients with amnesic MCI.
 ...
PMID:[Moderate cognitive impairment syndrome in cerebral vascular insufficiency]. 1579 3

The pyramidal CA1 neurons of the hippocampus are critically involved in spatial learning and memory. These neurons are especially vulnerable to cerebral ischemia, but in spite of this, it has been consistently difficult to show any learning and memory deficits in two-vessel occlusion models of global ischemia. Transient global ischemia was induced in adult male rats under general anaesthesia administered by artificial respiration to prevent respiratory arrest. Systemic blood pressure was reduced to below 50 mmHg by instant adjustments of the halothane concentration, before and during bilateral occlusion of the carotid arteries. Cerebral blood flow was monitored by laser-Doppler flowmetry. Dying neurons were detected by TUNEL at 14 days after ischemia and surviving neurons by NeuN at 14 and 125 days after ischemia. Learning and memory was assessed in a novel water maze with three successive left-right choices. Transient global ischemia produced a profound and selective degeneration of CA1 neurons at 14 days after ischemia. This degeneration was associated with severe impairments in learning at 13 days after ischemia and in memory, as tested 24 h afterwards. At 125 days after ischemia, there was no significant learning and memory impairment, whereas the number of CA1 neurons was increased. These results show that transient global ischemia induced by two-vessel occlusion may lead to severe, but transient, impairments in learning and memory using a novel water maze, and that restored learning and memory is associated with an increased number of CA1 neurons.
 ...
PMID:Profound but transient deficits in learning and memory after global ischemia using a novel water maze test. 1615 75

Recently, a potential neuroprotective effect of rimonabant, independent of the CB1 receptor interaction, has been proposed. In the present study, the role of transient receptor potential channel vanilloid subfamily member 1, named VR1, on neuroprotective effect of rimonabant, on global cerebral ischemia in gerbils, was investigated. Rimonabant (0.05-3 mg kg-1), given i.p. 5 min after recirculation, dose dependently antagonized the ischemia-induced decrease in electroencephalographic (EEG) total spectral power and restored relative frequency band distribution 7 days after ischemia. Rimonabant (0.125-0.5 mg kg-1) fully prevented ischemia-induced hyperlocomotion 1 day after ischemia and memory impairment evaluated in a passive avoidance task, 3 days after ischemia. At 7 days after ischemia, the survival of pyramidal cells, in the CA1 subfield, was respectively 91 and 96%, in the animals given rimonabant 0.25 and 0.5 mg kg-1, compared to the vehicle group. Higher doses were not protective. The protection induced by rimonabant followed a bell-shaped curve, the maximal active doses being 0.25 and 0.5 mg kg-1. Capsazepine (0.01 mg kg-1), a selective VR1 vanilloid receptor antagonist, completely reversed rimonabant-induced neuroprotective effects against EEG flattening, memory impairment and CA1 hippocampal neuronal loss. These findings suggest that VR1 vanilloid receptors are involved in rimonabant's neuroprotection even if other mechanisms can contribute to this effect.
 ...
PMID:Vanilloid VR1 receptor is involved in rimonabant-induced neuroprotection. 1644 89

Peroxynitrite involvement has been implicated in the neuronal damage. In the present study, we have investigated the neuroprotective effects of peroxynitrite decomposition catalyst (FeTMPyP) on global cerebral ischemia. Global cerebral ischemia-reperfusion (IR) injury was produced by 5 min occlusion of both common carotid arteries followed by reperfusion of 96 h in the adult male Mongolian gerbils. The extent of injury was assessed behaviorally by measuring neurological functions, locomotor activity, passive avoidance test and by histopathological evaluation of extent of damage to CA1 hippocampal pyramidal region. FeTMPyP (1 and 3 mgkg(-1), i.p., administered 30 min prior to ischemia) treatment improved the neurological functions, reduced the hyperlocomotion and memory impairment in IR challenged gerbils. The loss of neurons from the pyramidal layer of the CA1 region caused by global IR injury was attenuated with FeTMPyP. FeTMPyP also inhibited lipid peroxidation as evident from reduction in brain malondialdehyde levels. These results suggest that peroxynitrite decomposition catalyst may be effective neuroprotective agent for global cerebral ischemia.
 ...
PMID:Neuroprotective effects of FeTMPyP: a peroxynitrite decomposition catalyst in global cerebral ischemia model in gerbils. 1687 4


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>