Region-specific loss of zinc in the brain in pentylentetrazole-induced seizures and seizure susceptibility in zinc deficiency

Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52- 1 Yada, Shizuoka 422-8526, Japan.
Epilepsy Research (Impact Factor: 2.02). 08/2006; 70(1):41-8. DOI: 10.1016/j.eplepsyres.2006.03.002
Source: PubMed


The hippocampus is thought to be an epileptic focus in human temporal lobe epilepsy. Kainate-induced seizures decrease zinc concentrations in the hippocampus, which is also decreased in young mice fed a zinc-deficient diet for 4 weeks, and is enhanced by zinc deficiency. To understand zinc movement in the brain in epileptic seizures, zinc concentrations in the brain were measured in young mice after administration of pentylentetrazole, a GABAA receptor antagonist. Zinc concentration in the hippocampus and Timm's stain, with which histochemically reactive zinc in the presynaptic vesicle is detected, were decreased after the administration, suggesting that excessive excitation of zinc-containing glutamatergic neurons is induced in the hippocampus with pentylentetrazole. To clarify whether the decrease in zinc concentration in the hippocampus in zinc deficiency alter seizure susceptibility, furthermore, susceptibility to pentylentetrazole-induced seizures was examined in young mice fed the zinc-deficient diet for 4 weeks. The susceptibility, unlike susceptibility to kainate-induced seizures, was not appreciably enhanced by zinc deficiency. These results suggest that the decrease in zinc concentration in the hippocampus in zinc deficiency does not influence susceptibility to pentylentetrazole-induced seizures.

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    • "Variations in volume and architecture of the hippocampus have been observed in some brain diseases such as epilepsy, schizophrenia, mild cognitive impairment, and Alzheimer's disease (Scher et al. 2007). The hippocampus is thought to be an epileptic focus in human temporal lobe epilepsy (Takeda et al. 2006). "
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    ABSTRACT: In this study, we aimed to (1) propose landmarks for the hippocampus in a rat brain using an experimental study and (2) investigate hippocampus shape changes in a rat brain with epilepsy using the statistical shape analysis method. We have used the statistical shape analysis method to illustrate hippocampal shape deformation due to epilepsy. Statistical shape analysis is of increasing interest to the neuroimaging community because of its potential for locating morphological changes. Nineteen rat brains (ten healthy and nine epileptic) with hematoxylin and eosin images of the hippocampus were used. The results strongly indicated that the normalized hippocampal shape of the epileptic group was different from the nonepileptic group; deformation was seen most significantly in the medial regions of the cornu ammonis (CA1 and CA3) of the hippocampus. In conclusion, our landmark-based methodology detected regional differences in the hippocampus in epilepsy. This study may serve as an initial reference for future studies on shape alteration of the hippocampus associated with certain medical conditions.
    Full-text · Article · Dec 2009 · Anatomical Science International
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    • "Deux autres études menées en Italie et aux États-Unis, chez des enfants ayant une épilepsie pharmacorésistante ont montré qu'ils étaient à risque de malnutrition, mais aucune étude similaire n'a été réalisée jusqu'à présent chez les épileptiques non pharmacorésistants dans les pays développés [10] [16]. Chez l'animal, de nombreuses études ont été menées [18] [19] [20] [21] [22] [23] [24] [25] [26] [27] [28] [29] [30] [31] [32]. Leur but était de mettre en évidence le rôle éventuel de la dénutrition dans la survenue de crises d'épilepsie en explorant différentes pistes comme une carence en protéines ou en certains micronutriments. "
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    ABSTRACT: Zinc is present in high concentration in many structures of the limbic circuitry, however the role of zinc as a neuromodulator in such synapses is still uncertain. In this work, we verified the effects of zinc chelation in an animal model of epileptogenesis induced by amygdala rapid kindling. The basolateral amygdala was electrically stimulated ten times per day for 2 days. A single stimulus was applied on the third day. Stimulated animals received injections of PBS or the zinc chelator diethildythiocarbamate acid (DEDTC) before each stimulus series. Animals were monitored with video-EEG and were perfused 3h after the last stimulus for subsequent neo-Timm and Fluoro-Jade B analysis. Zinc chelation decreased the duration of both behavioral seizures and electrical after-discharges, and also decreased the EEG spikes frequency, without changing the progression of behavioral seizure severity. These results indicate that the zinc ion may have a facilitatory role during kindling progression.
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