Zinc content in discrete hippocampal and amygdaloid areas of the epilepsy (El) mouse and normal mice

Fukahori, Motofumi; Itoh, Masatoshi; Oomagari, Kiyoshi; Kawasaki, Hiroaki

doi:10.1016/0006-8993(88)90099-6

Cited by 40 publications

(10 citation statements)

References 24 publications

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“…Zn released from neuron terminals serves a neuromodulatory function, as suggested by the multiple selective actions of Zn on synaptic function and the potency of Zn ions to modulate numerous neurotransmitter receptors such as GABA, NMDA, and ion channels [5, 9, 22]. As a potential neuromodulator, Zn is capable of exerting effects that could either inhibit or promote neuronal excitability, suggesting the possibility of both pro- and anti-convulsant effects [23, 24]. In this study, Zn supplementation for 2 months did not show a protective effect on increased BBB permeability during convulsions.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Zinc Treatment on the Blood–Brain Barrier Permeability and Brain Element Levels During Convulsions

Yorulmaz

Seker

Demir

et al. 2012

Biol Trace Elem Res

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We evaluated the effect of zinc treatment on the blood–brain barrier (BBB) permeability and the levels of zinc (Zn), natrium (Na), magnesium (Mg), and copper (Cu) in the brain tissue during epileptic seizures. The Wistar albino rats were divided into four groups, each as follows: (1) control group, (2) pentylenetetrazole (PTZ) group: rats treated with PTZ to induce seizures, (3) Zn group: rats treated with ZnCl2 added to drinking water for 2 months, and (4) Zn + PTZ group. The brains were divided into left, right hemispheres, and cerebellum + brain stem regions. Evans blue was used as BBB tracer. Element concentrations were analyzed by inductively coupled plasma optical emission spectroscopy. The BBB permeability has been found to be increased in all experimental groups (p < 0.05). Zn concentrations in all brain regions in Zn-supplemented groups (p < 0.05) showed an increase. BBB permeability and Zn level in cerebellum + brain stem region were significantly high compared to cerebral hemispheres (p < 0.05). In all experimental groups, Cu concentration decreased, whereas Na concentrations showed an increase (p < 0.05). Mg content in all the brain regions decreased in the Zn group and Zn + PTZ groups compared to other groups (p < 0.001). We also found that all elements’ levels showed hemispheric differences in all groups. During convulsions, Zn treatment did not show any protective effect on BBB permeability. Chronic Zn treatment decreased Mg and Cu concentration and increased Na levels in the brain tissue. Our results indicated that Zn treatment showed proconvulsant activity and increased BBB permeability, possibly changing prooxidant/antioxidant balance and neuronal excitability during seizures.

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Section: Discussionmentioning

confidence: 99%

The Effects of Zinc Treatment on the Blood–Brain Barrier Permeability and Brain Element Levels During Convulsions

Yorulmaz

Seker

Demir

et al. 2012

Biol Trace Elem Res

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“…Seizures in EL mice commence with the onset of puberty, originate in or near the parietal lobe, and then spread to the hippocampus and to other brain regions (Ishida et al, 1993;Suzuki et al, 1991;Todorova et al, 1999;Uchibori et al, 2002). The observation that zinc concentration is significantly lower in the hippocampal dentate area of EL mice as compared to that of control mice (Fukahori et al, 1988) suggests that a decrease of hippocampal zinc may be involved in the pathophysiology of convulsive seizures in the EL mice. In these mice, zinc loading reduces seizure susceptibility, while susceptibility is increased by dietary zinc deficiency (Fukahori and Itoh, 1990).…”

Section: Epilepsymentioning

confidence: 97%

Zinc: The brain's dark horse

Bitanihirwe

Cunningham

2009

Synapse

240

154

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Zinc is a life-sustaining trace element, serving structural, catalytic, and regulatory roles in cellular biology. It is required for normal mammalian brain development and physiology, such that deficiency or excess of zinc has been shown to contribute to alterations in behavior, abnormal central nervous system development, and neurological disease. In this light, it is not surprising that zinc ions have now been shown to play a role in the neuromodulation of synaptic transmission as well as in cortical plasticity. Zinc is stored in specific synaptic vesicles by a class of glutamatergic or "gluzinergic" neurons and is released in an activity-dependent manner. Because gluzinergic neurons are found almost exclusively in the cerebral cortex and limbic structures, zinc may be critical for normal cognitive and emotional functioning. Conversely, direct evidence shows that zinc might be a relatively potent neurotoxin. Neuronal injury secondary to in vivo zinc mobilization and release occurs in several neurological disorders such as Alzheimer's disease and amyotrophic lateral sclerosis, in addition to epilepsy and ischemia. Thus, zinc homeostasis is integral to normal central nervous system functioning, and in fact its role may be underappreciated. This article provides an overview of zinc neurobiology and reviews the experimental evidence that implicates zinc signals in the pathophysiology of neuropsychiatric diseases. A greater understanding of zinc's role in the central nervous system may therefore allow for the development of therapeutic approaches where aberrant metal homeostasis is implicated in disease pathogenesis.

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“…1996). Zinc concentration in the hippocampal dentate area of seized EL (epilepsy) mice is significantly lower than that of control mice (Fukahori et al . 1988).…”

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confidence: 99%

Susceptibility to kainate‐induced seizures under dietary zinc deficiency

Takeda

Hirate

Tamano

et al. 2003

Journal of Neurochemistry

101

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Zinc homeostasis in the brain is altered by dietary zinc deficiency, and its alteration may be associated with the etiology and manifestation of epileptic seizures. In the present study, susceptibility to kainate-induced seizures was enhanced in mice fed a zinc-deficient diet for 4 weeks. When Timm's stain was performed to estimate zinc concentrations in synaptic vesicles, Timm's stain in the brain was attenuated in the zincdeficient mice. In rats fed the zinc-deficient diet for 4 weeks, susceptibility to kainate-induced seizures was also enhanced. When the release of zinc and neurotransmitters in the hippocampal extracellular fluid of the zinc-deficient rats was studied using in vivo microdialysis, the zinc concentration in the perfusate was less than 50% of that of the control rats and the increased levels of zinc by treatment with kainate were lower than the basal level in control rats, suggesting that vesicular zinc is responsive to dietary zinc deficiency. The levels of glutamate in the perfusate of the zinc-deficient rats were more increased than in the control rats, whereas the levels of GABA in the perfusate were not at all increased in the zincdeficient rats, unlike in the control rats. The present results demonstrate an enhanced release of glutamate associated with a decrease in GABA concentrations as a possible mechanism for the increased seizure susceptibility under zinc deficiency.

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Zinc content in discrete hippocampal and amygdaloid areas of the epilepsy (El) mouse and normal mice

Cited by 40 publications

References 24 publications

The Effects of Zinc Treatment on the Blood–Brain Barrier Permeability and Brain Element Levels During Convulsions

The Effects of Zinc Treatment on the Blood–Brain Barrier Permeability and Brain Element Levels During Convulsions

Zinc: The brain's dark horse

Susceptibility to kainate‐induced seizures under dietary zinc deficiency

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