Neurological and behavioral outcomes of focal cerebral ischemia in rats.

Wahl, Florence; Allix, Monique; Plotkine, Michel; Boulu, R

doi:10.1161/01.str.23.2.267

Cited by 169 publications

(109 citation statements)

References 27 publications

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“…Using the open fi eld test according to the criteria established at our institution 16 , we observed reduction of exploratory activity (rearing and sniffing) and of defecation on the 1st postoperative day in all animals of the ischemic groups. Despite differences in the elaboration and execution of the tests, our results agree with those reported by Wahl et al 6 regarding the absence of a correlation between the behavioral and histopathological changes.…”

Section: Discussionsupporting

confidence: 92%

“…Another study did not detect correspondence between the behavioral and histopathological effects provoked by coagulation of the MCA in rats 6 . Using the open fi eld test according to the criteria established at our institution 16 , we observed reduction of exploratory activity (rearing and sniffing) and of defecation on the 1st postoperative day in all animals of the ischemic groups.…”

Section: Discussionmentioning

confidence: 91%

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Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

Silva

Colli

Coimbra

et al. 2007

Arq. Neuro-Psiquiatr.

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-Objective: To study the neurobehavioral, biochemical and histopathological consequences of permanent focal brain ischemia, and the putative neuroprotective action of ketoprofen. Method: Onehundred-and-three Wistar rats divided into groups A and B were respectively submitted to 48 hours and 15 days of ischemia. Each group was divided into 4 subgroups: ischemic not treated, ischemic treated, sham not treated, and sham treated. Ischemic animals had the left middle cerebral artery coagulated. Ketoprofen was administered to treated subgroups 15 minutes before arterial coagulation (manipulation in the sham group). Results: Exploratory activity and defecation were reduced in all ischemic animals in the first postoperative days and constant histopathological changes were observed in each group. The total brain glutamate levels were higher in treated animals 48 hours after surgery. Conclusion: No clear parallelism among behavioral, biochemical and histopathological findings was observed. Ketoprofen demonstrated no neuroprotective effect on the behavioral or histopathological aspects of focal permanent brain ischemia.KEY WORDS: focal brain ischemia, rat, open field, glutamate, histopathology, neuroprotection, ketoprofen. Avaliação do efeito neuroprotetor do cetoprofeno em ratos submetidos à isquemia cerebral focal permanenteRESUMO -Objetivo: Estudar as conseqüências comportamentais, bioquímicas e histopatológicas da isquemia cerebral focal permanente e o possível efeito neuroprotetor do cetoprofeno. Método: Foram utilizados 103 ratos Wistar, divididos em grupos A e B, submetidos, respectivamente, a 48 horas e a 15 dias de isquemia. Cada grupo foi dividido em 4 subgrupos: isquêmico não tratado; isquêmico tratado; sham não tratado; sham tratado. Nos animais isquêmicos foi coagulada a artéria cerebral média esquerda. Os subgrupos tratados receberam cetoprofeno 15 minutos antes da oclusão ou manipulação arterial. Resultados: Os animais isquêmicos reduziram a atividade exploratória e as evacuações nos primeiros dias pós-operatórios e mostraram alterações histopatológicas constantes em cada grupo. As concentrações do glutamato total 48 horas após a cirurgia foram maiores nos animais tratados. Conclusão: Não houve um paralelismo entre os achados comportamentais, bioquímicos e histopatológicos. O cetoprofeno não apresentou efeito protetor contra isquemia cerebral focal permanente, nos aspectos comportamentais e histopatológicos.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 91%

Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

Silva

Colli

Coimbra

et al. 2007

Arq. Neuro-Psiquiatr.

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“…In these studies, 50 or 60 mg/kg G-CSF was administered via a single subcutaneous injection, and their findings formed the basis for the present study. However, changes in lesion volume do not always represent changes in functional outcome and, while some studies show that lesion size correlates with functional deficit (Rogers et al, 1997), others show it does not (Hattori et al, 2000;Reglodi et al, 2003;Wahl et al, 1992). In the current study, we measured lesion volume at 48 hours, and so it is not possible to rule out the possibility that G-CSF simply delayed the development of the lesion rather than reduced it.…”

Section: Discussionmentioning

confidence: 99%

G-CSF Reduces Infarct Volume and Improves Functional Outcome after Transient Focal Cerebral Ischemia in Mice

Gibson

Bath

Murphy

2005

J Cereb Blood Flow Metab

155

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Growth factors possess neuroprotective and neurotrophic properties in vitro, but few have been extensively studied in vivo after stroke. In the present study, we investigated the potential functional benefits of granulocyte colony-stimulating factor (G-CSF) administration after focal cerebral ischemia. Male mice underwent 60-minute middle cerebral artery occlusion (MCAO) and received G-CSF (50 lg/kg, subcutaneously) or vehicle (saline) at the onset of reperfusion. Granulocyte colony-stimulating factor-treated mice killed at 48 hours after MCAO revealed a 445% reduction (Po0.05) in lesion volume. In terms of body weight recovery, and in tests of motor (grid test and rotarod) and cognitive ability (water maze), MCAO significantly worsened the outcome in vehicletreated mice as compared with shams (Po0.05). However, G-CSF treatment was beneficial as, compared with vehicle, this significantly improved weight recovery and motor ability. This effect was most apparent on the water maze where G-CSF-treated mice were indistinguishable from shams in terms of acquiring the task. These results indicate long-term beneficial effects of a single dose of G-CSF administered on reperfusion, and illustrate the need to further investigate the mechanisms of G-CSF action.

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“…It has been suggested that damage to the cerebral cortex or to the striatum might thus also involve a deficit of learning and memory after MCA occlusion in the passive-avoidance task (Yamamoto et a!., 1988), the Y -maze task (Wahl et a!., 1992), or the water-maze task (Markgraf et a!., 1992). In the ra dial-maze task, the rats with single lesions of the caudate nucleus or neocortex showed cognitive def icits, but this deficit later gradually recovered (Cook and Kesner, 1988;Colombo et a!., 1989;Kesner et al, 1989;Packard et a!., 1989).…”

Section: Discussionmentioning

confidence: 99%

Long-Term Spatial Cognitive Impairment after Middle Cerebral Artery Occlusion in Rats: No Involvement of the Hippocampus

Okada

Nakanishi

Tamura

et al. 1995

J Cereb Blood Flow Metab

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Summary:The behavioral and neurochemical changes in the chronic phase of permanent occlusion of the right middle cerebral artery (MCA) in rats were investigated. One month after MCA occlusion, 23 rats were unable to solve a radial eight-arm maze task during an entire I-month period, whereas seven rats were able to solve this task. Three months after occlusion, 19 MCA-oc cluded rats failed to solve the task successfully again for at least I month (the cognitively impaired rats), whereas II MCA-occluded rats were able to solve it (the cogni tively unimpaired rats). The rats that underwent behav ioral testing were examined for any changes in the ace tylcholine (ACh) levels in the hippocampus using HPLC with electrochemical detection or the formation of long term potentiation (L TP) in the population spike of the hippocampal CAl field. The immunohistochemical distriPermanent unilateral middle cerebral artery (MCA) occlusion in rats is widely used as a model of focal cerebral ischemia. In the acute phase, this model selectively causes infarction in the ipsilateral cerebral cortex and caudate nucleus-putamen com plex (Tamura et aI., 1981 a; lizuka et aI., 1989). Af ter the infarction in the territory of the MCA, �2 weeks after MCA occlusion, progressive shrinkage occurs in the ipsilateral thalamus (Fujie et aI., 1990) Received March 31, 1994; final revision received October 14, 1995; accepted February 27, 1995. Address correspondence and reprint requests to Dr. Michihiro Fujiwara, Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka 814-01, Japan.Abbreviations used: MeA, middle cerebral artery; LTP, long term potentiation; MAP2, microtubule-associated protein 2; GFAP, glial fibrillary acidic protein. 1012bution of either the microtubule-associated protein 2 (MAP2) or glial fibrillary acidic protein (GF AP) in the hippocampus of the cognitively impaired rats was also studied. In the cognitively impaired rats, neither the sup pression of the induction of L TP, nor the degradation of MAP2, nor the increase in the GFAP immunoreactivity was observed in the hippocampus. The levels of ACh in the hippocampus did not change significantly among the cognitively impaired, unimpaired, and the sham-operated rats. These results suggest that MCA occlusion is capable of producing long-term spatial cognitive disturbance in rats without any evidence of neurobiological damage in the hippocampus. Key Words: Focal cerebral ischemia Memory-Long-term potentiation-Microtubule-asso ciated protein 2-Glial fibrillary acidic protein.

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Neurological and behavioral outcomes of focal cerebral ischemia in rats.

Cited by 169 publications

References 27 publications

Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

Evaluation of the neuroprotective effect of ketoprofen on rats submitted to permanent focal brain ischemia

G-CSF Reduces Infarct Volume and Improves Functional Outcome after Transient Focal Cerebral Ischemia in Mice

Long-Term Spatial Cognitive Impairment after Middle Cerebral Artery Occlusion in Rats: No Involvement of the Hippocampus

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