Tetanically released zinc inhibits hippocampal mossy fiber calcium, zinc and synaptic responses

Quinta‐Ferreira, Mário; Matias, Carlos M.

doi:10.1016/j.brainres.2005.04.006

Cited by 33 publications

(16 citation statements)

References 54 publications

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“…On the other hand, increases in the levels of chelatable (releasable) zinc pool can quickly perturb homeostasis, especially free zinc that is released from synaptic vesicles into the microenvironment of the synaptic cleft during synaptic stimulation. Under these conditions, abnormal zinc interactions with the postsynaptic element can profoundly affect neurotransmitter receptor function and thus alter synaptic transmission (Quinta-Ferreira and Matias, 2005; Weiss et al, 1993). Furthermore, compelling evidence suggests that released free zinc can coordinate with amyloid beta, stabilize the toxic oligomeric form, and promote their pathological targeting of the postsynaptic element (Deshpande et al, 2009; Noy et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Selective, quantitative measurement of releasable synaptic zinc in human autopsy hippocampal brain tissue from Alzheimer's disease patients

Bjorklund

Sadagoparamanujam

Taglialatela

2012

Journal of Neuroscience Methods

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Aberrant central nervous system zinc homeostasis has been reported in Alzheimer’s disease (AD). However, there are conflicting reports describing zinc concentration either increased or decreased in the brain of AD patients. Such discrepancies may be due to differences in the brain area examined, zinc detection method, and/or tissue composition. Furthermore, detection and measurement of the releasable zinc pool in autopsy tissue is difficult and usually unreliable. Obtaining an adequate assessment of this releasable zinc pool is of particular significance in AD research in that zinc can coordinate with and stabilize toxic amyloid beta oligomers, which are believed to play a key role in AD neuropathology. In addition, zinc released into the synaptic cleft can interact with the postsynaptic neurons causing altered signaling and synaptic dysfunction, which is a well established event in AD. The method presented here combines two approaches, biochemical fractionation and atomic absorption spectrophotometry, to allow, in addition to extracellular zinc concentration, the reliable and quantitative measurement of zinc specifically localized in synaptic vesicles, which contain the majority of the neuronal releasable zinc. Using this methodology, we found that synaptic vesicle zinc concentrations were increased in AD hippocampi compared to age-matched controls and that this increase in releasable zinc matched increased concentration of zinc in the extracellular space.

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Section: Discussionmentioning

confidence: 99%

Selective, quantitative measurement of releasable synaptic zinc in human autopsy hippocampal brain tissue from Alzheimer's disease patients

Bjorklund

Sadagoparamanujam

Taglialatela

2012

Journal of Neuroscience Methods

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“…[32][33][34][35] QuintaFerreira and Matias 36,37) report that Ca 2+ influx into mossy fibers by tetanic stimulation is inhibited by endogenous zinc. A sustained increase in Ca 2+ levels in CA3 pyramidal neurons is enhanced in the presence of 1-10 mM CaEDTA after regional delivery of 1 mM glutamate to dentate granule cells.…”

Section: Discussionmentioning

confidence: 99%

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

Takeda

Itoh

Tamano

et al. 2009

JOURNAL OF HEALTH SCIENCE

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To understand the physiological significance of endogenous zinc release under excess excitation in the hippocampus, in the present study, high K + -induced increase in extracellular glutamate and endogenous zinc action against its increase were examined in young rats fed a zinc-deficient diet for 2 weeks. When the ventral hippocampus was perfused by 100 mM KCl, the extracellular concentration of glutamate was more increased in zinc-deficient rats than the control rats. Calcium orange signal in mossy fiber boutons was more increased in slices from zincdeficient rats after delivery of tetanic stimuli (100 Hz, 5 sec) to the dentate granule cell layer. The decrease in FM4-64 signal, which is a measurement of exocytosis, in mossy fiber boutons was also enhanced in slices from zinc-deficient rats. These results suggest that the abnormal increase in extracellular glutamate in the hippocampus induced with high K + in zinc deficiency is due to the enhancement of exocytosis associated with affected Ca 2+ mobilization. The expression of GLT-1, a glial glutamate transporter, in the hippocampus was higher in zincdeficient rats, suggesting that GLT-1 protein increased serves to maintain the basal concentration of extracellular glutamate, which was not different between the control and zinc-deficient rats. On the other hand, the increase in extracellular glutamate concentration induced with high K + was enhanced in the presence of 1 mM CaEDTA, a membrane-impermeable zinc chelator, in both the control and zinc-deficient rats. It is likely that zinc released from glutamatergic neurons serves to suppress glutamate release under excess excitation in the hippocampus.

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“…After release into the synaptic cleft and diffusion, hippocampal mossy fiber Zn 2ϩ may modulate different pre-and postsynaptic mechanisms and may be taken up by Zn 2ϩ transport systems or enter the postsynaptic neurons. Recently, it has been reported that Zn 2ϩ released from mossy fibers activates presynaptic ATP-sensitive K ϩ channels (6,45). These authors concluded that the activation of such a channel type may rapidly hyperpolarize the cell, reducing Ca 2ϩ influx and glutamate release.…”

Section: Discussionmentioning

confidence: 99%

Episodic ataxia type 1 mutation F184C alters Zn²⁺-induced modulation of the human K⁺ channel Kv1.4-Kv1.1/Kvβ1.1

Imbrici

D’Adamo²,

Cusimano³

et al. 2007

American Journal of Physiology-Cell Physiology

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Tetanically released zinc inhibits hippocampal mossy fiber calcium, zinc and synaptic responses

Cited by 33 publications

References 54 publications

Selective, quantitative measurement of releasable synaptic zinc in human autopsy hippocampal brain tissue from Alzheimer's disease patients

Selective, quantitative measurement of releasable synaptic zinc in human autopsy hippocampal brain tissue from Alzheimer's disease patients

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

Episodic ataxia type 1 mutation F184C alters Zn²⁺-induced modulation of the human K⁺ channel Kv1.4-Kv1.1/Kvβ1.1

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Tetanically released zinc inhibits hippocampal mossy fiber calcium, zinc and synaptic responses

Cited by 33 publications

References 54 publications

Selective, quantitative measurement of releasable synaptic zinc in human autopsy hippocampal brain tissue from Alzheimer's disease patients

Selective, quantitative measurement of releasable synaptic zinc in human autopsy hippocampal brain tissue from Alzheimer's disease patients

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

Episodic ataxia type 1 mutation F184C alters Zn2+-induced modulation of the human K+ channel Kv1.4-Kv1.1/Kvβ1.1

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Episodic ataxia type 1 mutation F184C alters Zn²⁺-induced modulation of the human K⁺ channel Kv1.4-Kv1.1/Kvβ1.1