Measurement of presynaptic zinc changes in hippocampal mossy fibers

Quinta‐Ferreira, Mário; Matias, Carlos M.; Arif, Mona; Dionisio, José

doi:10.1016/j.brainres.2004.07.054

Cited by 31 publications

(22 citation statements)

References 52 publications

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“…Stimulation of organotypic cultures from rat hippocampus produced a cloud of green fluorescence as the released zinc bound an apometalloenzyme confirming the release of zinc from the culture [17]. A later study by Quinta-Ferreira and colleagues [20] demonstrated a release of zinc with each pulse of an action potential. Whilst there is now no doubt that zinc is released during synaptic activity, there is little consensus on the amount or duration of its existence in the synaptic cleft [21].…”

Section: Physiological Role Of Zinc In the Brainmentioning

confidence: 86%

The Role of Zinc in Alzheimer′s Disease

Watt

Whitehouse

Hooper

2010

International Journal of Alzheimer's Disease

105

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Zinc, the most abundant trace metal in the brain, has numerous functions, both in health and in disease. Zinc is released into the synaptic cleft of glutamatergic neurons alongside glutamate from where it interacts and modulates NMDA and AMPA receptors. In addition, zinc has multifactorial functions in Alzheimer's disease (AD). Zinc is critical in the enzymatic nonamyloidogenic processing of the amyloid precursor protein (APP) and in the enzymatic degradation of the amyloid-β (Aβ) peptide. Zinc binds to Aβ promoting its aggregation into neurotoxic species, and disruption of zinc homeostasis in the brain results in synaptic and memory deficits. Thus, zinc dyshomeostasis may have a critical role to play in the pathogenesis of AD, and the chelation of zinc is a potential therapeutic approach.

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Section: Physiological Role Of Zinc In the Brainmentioning

confidence: 86%

The Role of Zinc in Alzheimer′s Disease

Watt

Whitehouse

Hooper

2010

International Journal of Alzheimer's Disease

105

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“…LTP is the electrophysiological basis for synaptic plasticity. Quinta-Ferreira et al 18 demonstrated that vesicular zinc is required for induction of LTP in hippocampal mossy fiber synapses. The results in this study showed that the amplitude of LTP in hippocampal dentate gyrus in ZD rats decreased significantly than that in controls.…”

Section: Discussionmentioning

confidence: 99%

Depressed hippocampal MEK/ERK phosphorylation correlates with impaired cognitive and synaptic function in zinc-deficient rats

Jiang

Fang

Pang

et al. 2011

Nutritional Neuroscience

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An experiment was performed to observe changes of mitogen-activated protein kinase ERK (MEK)/extracellular signal-regulated kinase (ERK) signaling pathways in the hippocampus of zinc-deficient (ZD) rats and the correlation with cognitive dysfunction. Forty-four male weanling Wistar rats were randomly assigned to ZD (n = 22) and control (pair-fed, n = 22) groups. After a 4-week treatment, Y-maze was used to test the spatial memory of the rats. The long-term potentiation (LTP) in rat hippocampal dentate gyrus was observed simultaneously. pMEK, pERK1/2, and pCREB protein levels were examined by Western blot assays. The results demonstrated that the latency period in Y-maze was significantly shorter for the ZD rats. LTP amplitude in the ZD group decreased significantly compared with the control group. pMEK, pERK1/2, and pCREB protein expression of hippocampus in the ZD group decreased significantly. The results implicated a possibility that zinc deficiency-induced cognitive and synaptic impairment may be relevant to the MEK/ERK signaling pathway.

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“…In these terminals, zinc is colocalized with glutamate in synaptic vesicles. Zinc is released in a calciumdependent manner, after multiple (Assaf and Chung, 1984;Howell et al, 1984) or single (Quinta-Ferreira et al 2004) mossy fiber stimuli, then taken up by zinc transport processes (Cole et al, 1999) and refilled into synaptic vesicles (Sudhof, 1995;Clemens, 1996). Previous estimates of the peak synaptic zinc concentration during neuronal activity are 10 -30 M ( Thompson et al, 2000;Li et al, 2001b;Ueno et al, 2002) (but see Kay, 2003).…”

Section: Introductionmentioning

confidence: 99%

pH-Dependent Inhibition of Kainate Receptors by Zinc

Mott¹,

Benveniste²,

Dingledine³

2008

J. Neurosci.

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Kainate receptors contribute to synaptic plasticity and rhythmic oscillatory firing of neurons in corticolimbic circuits including hippocampal area CA3. We use zinc chelators and mice deficient in zinc transporters to show that synaptically released zinc inhibits postsynaptic kainate receptors at mossy fiber synapses and limits frequency facilitation of kainate, but not AMPA EPSCs during thetapattern stimulation. Exogenous zinc also inhibits the facilitatory modulation of mossy fiber axon excitability by kainate but does not suppress the depressive effect of kainate on CA3 axons. Recombinant kainate receptors are inhibited in a subunit-dependent manner by physiologically relevant concentrations of zinc, with receptors containing the KA1 subunit being sensitive to submicromolar concentrations of zinc. Zinc inhibition does not alter receptor desensitization nor apparent agonist affinity and is only weakly voltage dependent, which points to an allosteric mechanism. Zinc inhibition is reduced at acidic pH. Thus, in the presence of zinc, a fall in pH potentiates kainate receptors by relieving zinc inhibition. Acidification of the extracellular space, as occurs during repetitive activity, may therefore serve to unmask kainate receptor neurotransmission. We conclude that zinc modulation of kainate receptors serves an important role in shaping kainate neurotransmission in the CA3 region.

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Measurement of presynaptic zinc changes in hippocampal mossy fibers

Cited by 31 publications

References 52 publications

The Role of Zinc in Alzheimer′s Disease

The Role of Zinc in Alzheimer′s Disease

Depressed hippocampal MEK/ERK phosphorylation correlates with impaired cognitive and synaptic function in zinc-deficient rats

pH-Dependent Inhibition of Kainate Receptors by Zinc

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