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EEG Power Spectra Changes and Forebrain Ischemia in Rats

Published online by Cambridge University Press:  02 December 2014

Giuseppina Mariucci ,
Maria Antonietta Stasi ,
Roberto Taurelli ,
Paolo Nardò ,
Michela Tantucci ,
Licia Pacifici ,
Paolo Carminati  and
Maria Vittoria Ambrosini
Giuseppina Mariucci
Affiliation:
Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Perugia, Italy
Maria Antonietta Stasi
Affiliation:
SIGMA-TAU Industrie Farmaceutiche Riunite, Pomezia, Roma, Italy
Roberto Taurelli
Affiliation:
SIGMA-TAU Industrie Farmaceutiche Riunite, Pomezia, Roma, Italy
Paolo Nardò
Affiliation:
SIGMA-TAU Industrie Farmaceutiche Riunite, Pomezia, Roma, Italy
Michela Tantucci
Affiliation:
Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Perugia, Italy
Licia Pacifici
Affiliation:
SIGMA-TAU Industrie Farmaceutiche Riunite, Pomezia, Roma, Italy
Paolo Carminati
Affiliation:
SIGMA-TAU Industrie Farmaceutiche Riunite, Pomezia, Roma, Italy
Maria Vittoria Ambrosini
Affiliation:
Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Perugia, Italy
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Abstract

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Background:

Several animal models of cerebral ischemia have been developed to investigate both pathophysiology and pharmacological treatment. The aim of this study was to verify the prognostic value of EEG power spectra analysis in a two-vessel plus hypotension rat model of transient global ischemia.

Methods:

Spontaneously hypertensive rats (SHRs) and Wistar Kyoto rats (WKYs) were subjected to 20 min bilateral common carotid artery occlusion plus hypotension by sodium nitroprusside followed by reperfusion for seven days. Sham-operated animals served as controls. The changes after ischemia in EEG power spectra, and their relations with neuronal damage and astrocytic response were investigated.

Results:

The EEG analysis revealed that in SHRs and WKYs, ischemia produced a dramatic increase in delta activity and a decrease in theta, beta and alpha activities derived from both cortical and hippocampal areas. EEG activity reverted to normal values more quickly in WKYs than in SHRs which did not recover cortical and hippocampal alpha and beta activities even at six days of reperfusion. SHRs presented more severe damage and intense astrocytosis than WKYs in almost all the brain regions analyzed. In SHRs, hippocampal delta activity was positively correlated with the degree of neuronal necrosis and astrocytic activation, whereas theta, alpha and beta activities correlated negatively. No correlations were found in WKYs.

Conclusions:

These data indicate that the hippocampal bioelectrical activity recorded in SHRs from the beginning of reperfusion could be useful for predicting the ischemic outcome and evaluating the effects of pharmacological interventions.

Résumé:

RÉSUMÉ:Contexte:

Plusieurs modèles animaux ont été développés pour étudier la physiopathologie et le traitement pharmacologique de l’ischémie cérébrale. Le but de cette étude était d’évaluer la valeur pronostique de l’analyse du spectre électroencéphalographique de l’ischémie globale transitoire chez un modèle murin à deux vaisseaux avec hypotension.

Méthodes:

Des rats spontanément hypertendus (SHRs) et des rats Wistar Kyoto (WKYs) ont été soumis pendant 20 minutes à une occlusion bilatérale de la carotide commune avec hypotension au nitroprusside de sodium, suivie de reperfusion pendant sept jours. Des animaux ayant subi une intervention factice ont servi de témoins. Les changements du spectre électroencéphalographique après ischémie et leurs relations avec le dommage neuronal et la réponse astrocytaire ont été étudiés.

Résultats:

L’analyse de l’ÉEG a révélé que, chez les SHRs et les WKYs, l’ischémie a provoqué une augmentation dramatique de l’activité delta et une diminution de l’activité thêta, bêta et alpha, même après six jours de reperfusion. Les SHRs présentaient des dommages plus sévères et une astrocytose plus intense que les WKYs dans presque toutes les régions du cerveau analysées. Chez les SHRs, l’activité delta de l’hippocampe était corrélée positivement au degré de nécrose neuronale et à l’activation astrocytaire, alors qu’il existait une corrélation négative avec l’activité thêta, alpha et bêta. On n’a observé aucune corrélation chez les WKYs.

Conclusions:

Ces données indiquent que l’activité bioélectrique de l’hippocampe enregistrée chez les SHRs à partir du début de la reperfusion pourrait être utile pour prédire les conséquences de l’ischémie et évaluer les effets d’interventions pharmacologiques.

Type
Experimental Neurosciences
Information
Canadian Journal of Neurological Sciences , Volume 30 , Issue 1 , February 2003 , pp. 54 - 60
Copyright
Copyright © The Canadian Journal of Neurological 2003

References

1. Kusuda, K, Ibayashi, S, Sadoshima, S, Ishitsuka, T, Fujishima, M. Brain ischemia following bilateral carotid occlusion during development of hypertension in young spontaneously hypertensive rats: importance of morphologic changes of the arteries of the circle of Willis. Angiology 1996; 47: 455–465.CrossRefGoogle ScholarPubMed
2. Rubattu, S, Volpe, M, Kreutz, R, et al. Chromosomal mapping of quantitative trait loci contributing to stroke in a rat model of complex human disease. Nat Genet 1996; 13: 429–434.Google Scholar
3. Macdonell, RA, Donnan, GA, Bladin, PF, Berkovic, SF, Wriedt, CH. The electroencephalogram and acute ischemic stroke. Distinguishing cortical from lacunar infarction. Arch Neurol 1988; 45: 520–524.Google Scholar
4. Murri, L, Gori, S, Massetani, R, et al. Evaluation of acute ischemic stroke using quantitative EEG: a comparison with conventional EEG and CT SCAN. Neurophysiol Clin 1998; 28: 249–257.Google Scholar
5. Zimmer, C, Sampaolo, S, Shanker Sharma, H, Cervos-Navarro, J. Alterated glial fibrillary acidic protein immunoreactivity in rat brain following chronic hypoxia. Neuroscience 1991; 40: 353–361.Google Scholar
6. Petito, CK, Morgello, S, Felix, JC, Lesser, ML. The two patterns of reactive astrocytosis in postischemic rat brain. J Cereb Blood Flow Met 1990; 10: 850–859.Google Scholar
7. Gratton, JA, Sauter, A, Rudin, M, et al. Susceptibility to cerebral infarction in the stroke-prone spontaneously hypertensive rat is inherited as a dominant trait. Stroke 1998; 29: 690–694.Google Scholar
8. Rubattu, S, Volpe, M. Genetic basis of cerebrovascular accidents associated with hypertension. Cardiologia 1999; 44: 433–437.Google ScholarPubMed
9. Araki, H, Nojiri, M, Kawashima, K, Kimura, M, Aihara, H. Behavioral, electroencephalographic and histopathological studies on mongolian gerbils with occluded common carotid arteries. Physiol Behav 1986; 38: 89–94.Google Scholar
10. Janeczko, K. Expression of GFAP and vimentin in astrocytes proliferating in response to injury in the mouse cerebral hemisphere. Acombined autoradiographic and double immmunocytochemical study . Int J Dev Neurosci 1993; 11: 139–147.Google Scholar
11. Stringer, JL. Repeated seizures increase GFAP and Vimentin in hippocampus. Brain Res 1996; 717: 147–153.Google Scholar
12. Calvo, JL, Carbonell, AL, Boya, J. Coexpression of glial fibrillary acidic protein and vimentin in reactive astrocytes following brain injury in rats. Brain Res 1991; 566: 333–336.Google Scholar
13. Brint, S, Jacewicz, M, Kiessling, M, Tanabe, J, Pulsinelli, W. Focal brain ischemia in the rat: methods for reproducible neocortical infarction using tandem occlusion of the distal middle cerebral and ipsilateral commmon carotid arteries. J Cereb Blood Flow Metab 1988; 8: 474–485.Google Scholar
14. Kindy, MS, Bhat, AN, Bhat, NR. Transient ischemia stimulates glial fibrillary acid protein and vimentin gene expression in the gerbil neocortex, striatum and hippocampus. Mol Brain Res 1992; 13: 199–206.Google Scholar
15. Jordan, KG. Continuous EEG monitoring in the neuroscience intensive care unit and emergency department. J Clin Neurophysiol 1999; 16: 14–39.Google Scholar
16. Duverger, D, MacKenzie, ET. The quantification of cerebral infarction following focal ischemia in the rat: influence of strain, arterial pressure, blood glucose concentration and age. J Cereb Blood Flow Metab 1988; 8: 449–461.Google Scholar
17. Chen, H, Chopp, M, Schultz, L, Bodzin, G, Garcia, JH. Sequential neuronal and astrocytic changes after transient middle cerebral artery occlusion in the rat. J Neurol Sci 1993; 118: 109–116.CrossRefGoogle ScholarPubMed
18. Suzuki, R, Yamaguchi, T, Li, CL, Klatza, I. The effects of 5-minute ischemia in Mongolian gerbils: II.Changes of spontaneous neuronal activity in cerebral cortex and CA1 sector of Hippocampus. Acta Neuropathol 1983; 60: 217–222.Google Scholar
19. Gambelunghe, C, Mariucci, G, Bruschelli, G, et al. Response variability to ischemic injury in the Mongolian gerbil: an electroencephalographic and behavioral study. Ital J Neurol Sci 1996; 17: 219–225.Google Scholar
20. Sainio, K, Stenberg, D, Keskimaki, I, Muuronen, A, Kaste, M. Visual and spectral EEG analysis in the evaluation of outcome in patients with ischemic brain infarction. Electroenceph Clin Neurophysiol 1983; 56: 117–124.CrossRefGoogle ScholarPubMed
21. Ginsberg, MD, Busto, R. Rodent models of cerebral ischemia. Stroke 1989; 20: 1627–1642.Google Scholar
22. Hunter, AJ, Green, AR, Cross, AJ. Animal models of acute ischaemic stroke: can they predict clinically successful neuroprotective drugs? Trends Pharmacol Sci 1995; 16: 123–128.Google Scholar
23. Yanagihara, T. Experimental Stroke in gerbils: correlation of clinical, pathological and electroencephalographic findings and protein syntesis. Stroke 1978; 9: 155–159.Google Scholar
24. Schiffer, D, Giordana, MT, Cavalla, P, Vigliani, MC, Attanasio, A. Immunohistochemistry of glial reaction after injury in the rat: double stainings and markers of cell proliferation. Int J Devl Neurosci 1993; 11: 269–280.Google Scholar
25. Fujishima, M, Tamaki, K, Nakatomi, Y, et al. Experimental cerebral ischemia in spontaneously hypertensive rats (SHR): importance of degree of hypertension. Stroke 1980; 11: 612–616.Google Scholar
26. Coyle, P. Different susceptibilities to cerebral infarction in spontaneusly hypertensive (SHR) and normotensive Sprague-Dawley rats. Stroke 1986; 17: 520–525.Google Scholar
27. Ogata, J, Fujishima, M, Morotomi, Y, Omae, T. Cerebral infarction following bilateral carotid artery ligation in normotensive and spontaneously hypertensive rats: a pathological study. Stroke 1976; 7: 54–60.CrossRefGoogle ScholarPubMed