Secondary ion microanalysis in the study of cobalt-induced epilepsy in the rat

Trottier, Suzanne; Truchet, M.; Laroudie, C.

doi:10.1016/0014-4886(82)90204-7

Cited by 24 publications

(10 citation statements)

References 22 publications

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“…However, this modification might be attributed to residual amounts of cobalt in the homogenates used in the assay. It has been shown that significant amounts of cobalt are still present in the cerebral cortex of lesioned rats 90 days after cobalt deposit (Trottier et aL, 1982). Although in this study, the cortical content of metal was not determined, our experiments indicate that concentrations of cobalt as low as 1 nM can induce a 50o/o decrease in the affinity offl-adrenoceptor sites for 3H-DHA.…”

Section: Discussioncontrasting

confidence: 51%

Chronic cobalt-induced epilepsy: Noradrenaline ionophoresis and adrenoceptor binding studies in the rat cerebral cortex

Bregman

Saux

Trottier

et al. 1985

J. Neural Transmission

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Several studies indicate that brain noradrenaline (NA) depletion facilitates the occurrence of epileptogenic syndromes in various animal models. In cobalt-induced epilepsy in the rat activity is associated with a cortical NA denervation. In order to search for cortical adrenoceptor modifications, inonophoretic studies and adrenoceptor binding assays were performed. At the period of maximal seizure activity, there was a significant supersensitivity of cortical neurons to the ionophoretic application of NA. An increase in the density of beta-adrenoceptor binding sites was observed. No modification in alpha 1- and alpha 2-adrenoceptor binding sites was found. This suggests that in cobalt-induced epilepsy there is a denervation supersensitivity which rests on a selective involvement of beta-adrenoceptors.

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Section: Discussioncontrasting

confidence: 51%

Chronic cobalt-induced epilepsy: Noradrenaline ionophoresis and adrenoceptor binding studies in the rat cerebral cortex

Bregman

Saux

Trottier

et al. 1985

J. Neural Transmission

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“…Spread of iron to the contralateral side may be responsible for the effect. Although spread of iron to the contralateral side from the ipsilateral focus in the case of iron experimental epileptogenesis has not been studied, spread of cobalt from the side of its application to the contralateral epileptogenic focus has now been observed in cobalt experimental epileptogenesis (Trottier et al, 1982(Trottier et al, , 1983 although previously it was not believed to occur (Myers, 1974;Emson and Joseph, 1975).…”

Section: Days Aftermentioning

confidence: 99%

Lipid Peroxidation and Glutathione Peroxidase, Glutathione Reductase, Superoxide Dismutase, Catalase, and Glucose‐6‐Phosphate Dehydrogenase Activities in FeCl₃‐Induced Epileptogenic Foci in the Rat Brain

1990

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This study investigated the relationship between lipid peroxidation, subsequent activation of antioxidative enzymes, and development of iron-induced epilepsy in the rat. Epileptic foci were produced in rat cerebral cortex by intracortical injection of ferric chloride (FeCl3). The epileptic foci were identified by electrocorticography (ECoG). Epileptiform ECoG activity was shown to occur in the contralateral homotopic cerebral cortex as well. We measured levels of lipid peroxides and changes in the activities of the enzymes: superoxide dismutase (SOD), glutathione peroxidase (GP), glutathione reductase (GR), catalase (CA), and glucose-6-phosphate dehydrogenase (G6P) in the epileptogenic focus (both ipsilateral and contralateral) at days 3, 8, 15, and 23 after FeCl3 injection. Biochemical estimations were made in subcellular fractions, and changes in the ipsilateral site were compared with those in the contralateral site. The results of this study showed that large increases in lipid peroxidation were associated with development and buildup of the ECoG epileptiform discharges. Lipid peroxides increased in the ipsilateral focus by approximately 100% as compared with control. In the contralateral site, however, the increase in lipid peroxides was marginal only. The increase in lipid peroxidation was concomitant with development of the high level of epileptiform activity. The time course of changes in lipid peroxidation paralleled the time course of development and persistence of the epileptiform activity. Regarding changes in the enzyme activities accompanying development of iron epilepsy, the data showed that although SOD and G6P increased by approximately 60% and GR increased by approximately 40%, the increases in the enzyme GP and CA were much lower, less than 20%. Thus, comparatively less increase in CA and GP activities produces a deficiency of these two enzymes in the iron (ipsilateral) focus. Among the various biochemical disturbances that have been identified as involved in epileptogenesis, peroxidative injury resulting from lipid peroxidation in neural plasma membrane may be causally related to development of paroxysmal epileptiform activity in the iron focus. Since GP is an enzyme of major importance in detoxification of lipid peroxides in the brain, based on the results presented in this article, it appears reasonable to suggest that GP deficiency causes lipid peroxidation to increase tremendously during iron epileptogenesis.

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“…Cobalt is an essential trace metal known to be a cofactor of vitamin B 12 (Roth et al, 1996) and other cobalt‐containing enzymes (Kobayashi & Shimizu, 1999). Excessive cobalt exposure as demonstrated via direct intracranial applications induces seizures in mice, rats, cats, and monkeys (Dow et al, 1962; Mutani, 1967; Grimm et al, 1970; Babb et al, 1974; Willmore et al, 1975; Butler et al., 1977; Farjo & McQueen, 1979; Brown et al, 1980; Ross & Craig, 1981; Trottier et al, 1982; Zhao et al, 1985; Veregge & Frost, 1988; Tamargo et al, 2002; Chang et al, 2004; Fischer et al, 2004; Velišek, 2006). The cobalt‐induced seizures share some common features with human epilepsies regarding intermittent occurrence, paroxysmal nature, and response to anticonvulsants (Craig & Colasanti, 1986).…”

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confidence: 99%

Cellular mechanisms of cobalt‐induced hippocampal epileptiform discharges

Hsiang

et al. 2009

Epilepsia

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SUMMARYPurpose: To explore the cellular mechanisms of cobalt-induced epileptiform discharges in mouse hippocampal slices. Methods: Hippocampal slices were prepared from adult mice and briefly exposed to a CoCl 2 -containing external solution. Population and single cell activities were examined via extracellular and whole-cell patch recordings. Results: Brief cobalt exposure induced spontaneous, ictal-like discharges originating from the CA3 area. These discharges were suppressed by anticonvulsants, gap junction blockers, or by raising extracellular Ca 2+ , but their generation was not associated with overall hyperexcitability or impairment in GABAergic inhibition in the CA3 circuit. Electroencephalographic ictal discharges of similar waveforms were observed in behaving rats following intrahippocampal cobalt infusion. Discussion: Mechanisms involving activity-dependent facilitation of gap junctional communication may play a major role in cobalt-induced epileptiform discharges.

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Secondary ion microanalysis in the study of cobalt-induced epilepsy in the rat

Cited by 24 publications

References 22 publications

Chronic cobalt-induced epilepsy: Noradrenaline ionophoresis and adrenoceptor binding studies in the rat cerebral cortex

Chronic cobalt-induced epilepsy: Noradrenaline ionophoresis and adrenoceptor binding studies in the rat cerebral cortex

Lipid Peroxidation and Glutathione Peroxidase, Glutathione Reductase, Superoxide Dismutase, Catalase, and Glucose‐6‐Phosphate Dehydrogenase Activities in FeCl₃‐Induced Epileptogenic Foci in the Rat Brain

Cellular mechanisms of cobalt‐induced hippocampal epileptiform discharges

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Secondary ion microanalysis in the study of cobalt-induced epilepsy in the rat

Cited by 24 publications

References 22 publications

Chronic cobalt-induced epilepsy: Noradrenaline ionophoresis and adrenoceptor binding studies in the rat cerebral cortex

Chronic cobalt-induced epilepsy: Noradrenaline ionophoresis and adrenoceptor binding studies in the rat cerebral cortex

Lipid Peroxidation and Glutathione Peroxidase, Glutathione Reductase, Superoxide Dismutase, Catalase, and Glucose‐6‐Phosphate Dehydrogenase Activities in FeCl3‐Induced Epileptogenic Foci in the Rat Brain

Cellular mechanisms of cobalt‐induced hippocampal epileptiform discharges

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Lipid Peroxidation and Glutathione Peroxidase, Glutathione Reductase, Superoxide Dismutase, Catalase, and Glucose‐6‐Phosphate Dehydrogenase Activities in FeCl₃‐Induced Epileptogenic Foci in the Rat Brain