Determination of Zinc, Copper, Iron, and Manganese in Different Regions of Lamb Brain

Bakırdere, Sezgin; Kizilkan, Nese; Yaman, Mehmet

doi:10.1007/s12011-010-8804-0

Cited by 11 publications

(3 citation statements)

References 37 publications

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“…Previous reports suggest concentrations of zinc in the sheep brain to be approximately in the range of 4–10 µg/g, depending on the region studied, and the manganese concentrations in the range of 0.3–0.6 µg/g [38], [39] consistent with the control data here. While there is little knowledge of metal amounts in the brains of sheep affected by disease, it has been shown that zinc and manganese concentrations are elevated by approximately 22% in scrapie-infected sheep [38].…”

Section: Discussionsupporting

confidence: 91%

Increased Zinc and Manganese in Parallel with Neurodegeneration, Synaptic Protein Changes and Activation of Akt/GSK3 Signaling in Ovine CLN6 Neuronal Ceroid Lipofuscinosis

et al. 2013

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Mutations in the CLN6 gene cause a variant late infantile form of neuronal ceroid lipofuscinosis (NCL; Batten disease). CLN6 loss leads to disease clinically characterized by vision impairment, motor and cognitive dysfunction, and seizures. Accumulating evidence suggests that alterations in metal homeostasis and cellular signaling pathways are implicated in several neurodegenerative and developmental disorders, yet little is known about their role in the NCLs. To explore the disease mechanisms of CLN6 NCL, metal concentrations and expression of proteins implicated in cellular signaling pathways were assessed in brain tissue from South Hampshire and Merino CLN6 sheep. Analyses revealed increased zinc and manganese concentrations in affected sheep brain in those regions where neuroinflammation and neurodegeneration first occur. Synaptic proteins, the metal-binding protein metallothionein, and the Akt/GSK3 and ERK/MAPK cellular signaling pathways were also altered. These results demonstrate that altered metal concentrations, synaptic protein changes, and aberrant modulation of cellular signaling pathways are characteristic features in the CLN6 ovine form of NCL.

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Section: Discussionsupporting

confidence: 91%

Increased Zinc and Manganese in Parallel with Neurodegeneration, Synaptic Protein Changes and Activation of Akt/GSK3 Signaling in Ovine CLN6 Neuronal Ceroid Lipofuscinosis

et al. 2013

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“…Most of the work exploring the role of Cu in synaptic transmission and plasticity has been conducted in the hippocampus. ATP7A is expressed at high levels in the pyramidal neurons and interneurons of the neocortex and hippocampus (Schlief et al, 2005; Niciu et al, 2006), where Cu content is also relatively high (Rajan et al, 1976; Bakirdere et al, 2010). Cu is released from cultured hippocampal neurons in an N‐methyl‐D‐aspartate (NMDA) receptor‐dependent manner, and stimulation of NMDA receptors results in the trafficking of ATP7A out of the late Golgi into dendrites (Schlief et al, 2005; Dodani et al, 2011).…”

Section: Brain Copper Homeostasis: From Serum To Synapsementioning

confidence: 99%

Copper signaling in the mammalian nervous system: Synaptic effects

Gaier

Eipper

Mains

2012

J of Neuroscience Research

183

151

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Copper (Cu) is an essential metal present at high levels in the CNS. Its role as a co-factor in mitochondrial ATP production and in other essential cuproenzymes is well defined. Menkes and Wilson’s diseases are severe neurodegenerative conditions that demonstrate the importance of Cu transport into the secretory pathway. Brain levels of Cu, which is almost entirely protein bound, exceed extracellular levels by more than a hundred-fold. Cu stored in the secretory pathway is released in a Ca2+-dependent manner and can transiently reach concentrations over 100 µM at synapses. The ability of low µM levels of Cu to bind to and modulate the function of γ-aminobutyric acid type A (GABAA) receptors, N-methyl-D-aspartate (NMDA) receptors and voltage-gated Ca2+ channels contributes to its effects on synaptic transmission. Cu also binds to amyloid precursor protein and prion protein; both proteins are found at synapses and brain Cu homeostasis is disrupted in mice lacking either protein. Especially intriguing is the ability of Cu to affect AMP-activated protein kinase (AMPK), a monitor of cellular energy status. Despite this, few investigators have examined the direct effects of Cu on synaptic transmission and plasticity. Although the variability of results demonstrates complex influences of Cu that are highly method-sensitive, these studies nevertheless strongly support important roles for endogenous Cu and new roles for Cu-binding proteins in synaptic function/plasticity and behavior. Further study of the many roles of Cu in nervous system function will reveal targets for intervention in other diseases in which Cu homeostasis is disrupted.

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“…Brain iron levels were measured by Barkidere's method (Bakirdere et al 2010). Samples of brain tissues from the frontal and temporal lobe were immediately digested.…”

Section: Brain Biochemical Measurementsmentioning

confidence: 99%

Fatty acids rehabilitated long-term neurodegenerative: like symptoms in olfactory bulbectomized rats

Yehuda

Rabinovitz

2014

J Neural Transm

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Our previous study demonstrated that an olfactory bulbectomy in rats induced short-term, multifaceted, devastating Alzheimer's-like effects, which included cognitive impairment, hyperactivity, hyperthermia, and increased levels of homocysteine and pro-inflammatory cytokines, including IL-17A. In addition, the rats exhibited an increase in the hyperphosphorylation of brain Tau proteins and in the number of neurofibrillary tangles. Here, we examined the long-term effects of the surgery and found that olfactory bulbectomy also rendered the rats to become anemic with brain iron overload. Additionally, a significant reduction in the membrane fluidity index in frontal cortex synaptosomes was found. Treatment with a mixture of n - 3/n - 6 of fatty acids restored the unwanted effect. The beneficial effects of fatty acids are mediated via the effects of fatty acids on the neuronal membrane structure and fluidity. These findings are similar to Alzheimer's symptoms, which suggest this model can be used as an animal model for Alzheimer's disease. We recommend using this model to scan potential new anti-Alzheimer's drugs.

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Determination of Zinc, Copper, Iron, and Manganese in Different Regions of Lamb Brain

Cited by 11 publications

References 37 publications

Increased Zinc and Manganese in Parallel with Neurodegeneration, Synaptic Protein Changes and Activation of Akt/GSK3 Signaling in Ovine CLN6 Neuronal Ceroid Lipofuscinosis

Increased Zinc and Manganese in Parallel with Neurodegeneration, Synaptic Protein Changes and Activation of Akt/GSK3 Signaling in Ovine CLN6 Neuronal Ceroid Lipofuscinosis

Copper signaling in the mammalian nervous system: Synaptic effects

Fatty acids rehabilitated long-term neurodegenerative: like symptoms in olfactory bulbectomized rats

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