High K+-induced Increase in Extracellular Glutamate in Zinc Deficiency and Endogenous Zinc Action

Takeda, Atsüshi; Itoh, Hiromasa; Tamano, Haruna; Oku, Naoto

doi:10.1248/jhs.55.405

Cited by 2 publications

(1 citation statement)

References 40 publications

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“…The physiological significance of zinc release under excess excitation of zincergic neurons is also examined by an in vivo microdialysis experiment. The increase in extracellular glutamate concentration induced with 100 mM KCl was significantly enhanced in the presence of 1-mM CaEDTA in both the control and zinc-deficient rats [81]. Furthermore, chelation of endogenous zinc by CaEDTA causes a significant increase in ischemic cell death in hippocampal slice cultures [51].…”

Section: Zn 2+ Signaling In Glutamate Excitotoxicitymentioning

confidence: 99%

Zinc Signaling in the Hippocampus and Its Relation to Pathogenesis of Depression

Takeda

2010

Mol Neurobiol

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Zinc is released from glutamatergic (zincergic) neuron terminals in the brain, followed by the increase in Zn²⁺ concentration in the intracellular (cytosol) compartment as well as that in the extracellular compartment. Intracellular Zn²⁺ concentration mainly increases through calcium-permeable channels and serves as Zn²⁺ signal as well as extracellular Zn²⁺ concentration. Hippocampal Zn²⁺ signaling may participate in synaptic plasticity such as long-term potentiation and cognitive function. On the other hand, subclinical zinc deficiency is common in the old who might be more susceptible to depression. Zinc deficiency causes abnormal glucocorticoid secretion and increases depression-like behavior in animals. Neuropsychological symptoms are observed prior to the decrease in Zn²⁺ signal in the hippocampus under zinc deficiency. This paper summarizes that hippocampal Zn²⁺ signaling serves to maintain healthy brain and that glucocorticoid signaling, which is responsive to zinc homeostasis in the living body, is linked to the pathophysiology of depression.

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Section: Zn 2+ Signaling In Glutamate Excitotoxicitymentioning

confidence: 99%

Zinc Signaling in the Hippocampus and Its Relation to Pathogenesis of Depression

Takeda

2010

Mol Neurobiol

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Preventive Effect of 3,5-dihydroxy-4-methoxybenzyl Alcohol (DHMBA) and Zinc, Components of the Pacific Oyster Crassostrea gigas, on Glutamatergic Neuron Activity in the Hippocampus

Tamano

Shakushi

Watanabe³

et al. 2015

The Biological Bulletin

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The effects of 3,5-dihydroxy-4-methoxybenzyl alcohol (DHMBA), and zinc--both components of the Pacific oyster Crassostrea gigas--were examined by glutamatergic neuron activity in rats in an in vivo microdialysis experiment and an in vitro brain slice experiment. The basal concentration of extracellular glutamate in the hippocampus was decreased under hippocampal perfusion with DHMBA (1 mmol l(-1)) or ZnCl2 (μmol l(-1)), indicating that DHMBA and Zn(2+) suppress glutamatergic neuron activity under basal (static) conditions. To assess the preventive effect of DHMBA and Zn(2+) on glutamate release from neuron terminals, brain slices were pretreated with DHMBA (1 mmol l(-1)) or ZnCl2 (100 nmol l(-1)) for 1 h, then stimulated with high K(+). A high, K(+)-induced increase in extracellular Zn(2+) level, an index of glutamate release, was suppressed with pretreatment with DHMBA or zinc. A high, K(+)-induced increase in intracellular Ca(2+) level was also suppressed with pretreatment with DHMBA or Zn(2+). These results suggest that DHMBA and Zn(2+), previously taken up in the hippocampal cells, suppress high, K(+)-induced glutamate release in the hippocampus, probably via presynaptic suppression of intracellular Ca(2+) signaling. It is likely that Zn(2+) and DHMBA play a preventive role in suppressing excess glutamatergic neuron activity in rats and mice.

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High K+-induced Increase in Extracellular Glutamate in Zinc Deficiency and Endogenous Zinc Action

Cited by 2 publications

References 40 publications

Zinc Signaling in the Hippocampus and Its Relation to Pathogenesis of Depression

Zinc Signaling in the Hippocampus and Its Relation to Pathogenesis of Depression

Preventive Effect of 3,5-dihydroxy-4-methoxybenzyl Alcohol (DHMBA) and Zinc, Components of the Pacific Oyster Crassostrea gigas, on Glutamatergic Neuron Activity in the Hippocampus

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