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Figure 3 Open in figure viewer PowerPoint. Figure 4 Open in figure viewer PowerPoint. Figure 5 Open in figure viewer PowerPoint. Figure 6 Open in figure viewer PowerPoint. Those cellular dysregulations all contribute to promote muscle apoptosis. Supporting Information Filename Description acelsupSupinfo. Adhihetty, P. American Journal of Physiology. Cell Physiology , , C — C Crossref PubMed Google Scholar. Volume 18 , Issue 5 October e Figures References Related Information.

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Returning user. Request Username Can't sign in? Forgot your username? Enter your email address below and we will send you your username. Significantly, cholinergic neurons that had lost their calbindin in the course of normal aging were those that selectively degenerated in AD, while calbindin-containing neighboring neurons were virtually resistant to the process of tangle formation, a hallmark of the disease Riascos et al. Another study reported that over-expression of calbindin in presenilin 1 mutant neurons was sufficient to prevent apoptosis Guo et al.

These findings are consistent with earlier findings suggesting that calbindin-positive hippocampal neurons are more resistant against oxidative stress Mattson et al. More work in this direction would greatly enhance our ability to selectively intervene in order to modulate the vulnerability of distinct neuronal populations. The idea that mitochondria could be directly involved in the pathogenesis of PD comes from the early accidental observation that 1-methylphenyl-1,2,3,6-tetrahydropyridine MPTP , an inhibitor of the mitochondrial respiratory chain complex I, causes Parkinson-like symptoms Langston and Ballard, Later on, it was also demonstrated that DA neurons from PD patients show massive accumulation of mitochondrial DNA mtDNA deletions that impair the function of the respiratory chain complexes Exner et al.

Some clues as to the selective vulnerability of this population arise from the fact that DA neurons of the substantia nigra display unusual physiological properties. First, unlike most other neurons in the brain, they are autonomously active, generating regular action potentials in the absence of synaptic input Grace and Bunney, This pacemaking activity is thought to maintain physiological levels of dopamine in regions they innervate, particularly the striatum Romo and Schultz, Second, DA neurons of the substantia nigra display an elaborate axonal network Matsuda et al.

As a result, the mitochondrial density in their somatic and dendritic regions is very low compared to other neuronal types Liang et al. At least 13 gene loci and 9 genes have been linked to both autosomal dominant and recessive forms of PD Lesage and Brice, Mitochondrial dysfunction has been described for mutants of all these genes Lesage and Brice, DJ-1 is a multitask protein that, in addition to its main role as an antioxidant Taira et al.

As these results were obtained in vitro using non-neuronal cell lines, their relevance to DA neuron physiology and pathology remains to be examined. However, consistently, numerous reports showed that PINK1-deficient cells have impaired mitochondrial membrane potential and enhanced sensitivity to the toxic effects of mitochondrial complex I inhibitors Wood-Kaczmar et al.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potentialconflict of interest. Akundi, R. Increased mitochondrial calcium sensitivity and abnormal expression of innate immunity genes precede dopaminergic defects in Pink1-deficient mice.

Arbuthnott, G. Space, time and dopamine. Trends Neurosci. Artola, A. Long-term depression of excitatory synaptic transmission and its relationship to long-term potentiation. Atluri, P. Delayed release of neurotransmitter from cerebellar granule cells. Pubmed Abstract Pubmed Full Text. Bacman, S. Mitochondrial involvement in amyotrophic lateral sclerosis: trigger or target? CrossRef Full Text. Baines, C. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death.

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Cellular Mechanism for Calcium Transfer and Homeostasis ebook | fodusulogi.tk

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Baker, P. The voltage-sensitivity of Na—Ca exchange in the squid axon. Ban, T. Nimodipine in the treatment of old age dementias. Psychiatry 14, — Barnes, C. Normal aging: regionally specific changes in hippocampal synaptic transmission. Barrett, E. The kinetics of transmitter release at the frog neuromuscular junction. Basso, E. Properties of the permeability transition pore in mitochondria devoid of cyclophilin D.

Beal, M. Behne, M. Bernard-Marissal, N. Reduced calreticulin levels link endoplasmic reticulum stress and Fas-triggered cell death in motoneurons vulnerable to ALS. Bernardi, P. Mitochondria and cell death. Mechanistic aspects and methodological issues. Berridge, M. Neuronal calcium signaling. Neuron 21, 13— Bezprozvanny, I.

Calcium signaling and neurodegenerative diseases. Trends Mol. Blaustein, M. Bliss, T. A synaptic model of memory: long-term potentiation in the hippocampus. Nature , 31— Bodhinathan, K. Redox sensitive calcium stores underlie enhanced after hyperpolarization of aged neurons: role for ryanodine receptor mediated calcium signaling.

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Bonci, A. L-type calcium channels mediate a slow excitatory synaptic transmission in rat midbrain dopaminergic neurons. Braunewell, K. Intracellular neuronal calcium sensor proteins: a family of EF-hand calcium-binding proteins in search of a function. Cell Tissue Res. Burgoyne, R. Buxbaum, J. A role for calsenilin and related proteins in multiple aspects of neuronal function. Calsenilin: a calcium-binding protein that interacts with the presenilins and regulates the levels of a presenilin fragment.

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Cellular Mechanism for Calcium Transfer and Homeostasis

Mitochondria, calcium and cell death: a deadly triad in neurodegeneration. Acta , — Chalfie, M. The identification and suppression of inherited neurodegeneration in Caenorhabditis elegans. Chameau, P. Pflugers Arch.


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Chan, C. Chan, S. Presenilin-1 mutations increase levels of ryanodine receptors and calcium release in PC12 cells and cortical neurons. Cheung, K. Contreras, L. Mitochondria: the calcium connection. Csordas, G. Structural and functional features and significance of the physical linkage between ER and mitochondria.

Damiano, M. Danzer, K. Different species of alpha-synuclein oligomers induce calcium influx and seeding. Davare, M. Dekkers, J. Over-expression of parvalbumin in transgenic mice rescues motoneurons from injury-induced cell death. Neuroscience , — Del Arco, A. Characterization of a second member of the subfamily of calcium-binding mitochondrial carriers expressed in human non-excitable tissues. Molecular cloning of Aralar, a new member of the mitochondrial carrier superfamily that binds calcium and is present in human muscle and brain. Deyo, R. Nimodipine ameliorates aging-related changes in open-field behaviors of the rabbit.

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Aging Cell 6, — Calcium dysregulation in the aging brain. Neuroscientist 8, — Hippocampus 7, — Furuichi, T. Furukawa, K. Plasma membrane ion permeability induced by mutant alpha-synuclein contributes to the degeneration of neural cells. Gallagher, M.

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Neuroreport 8, — Guzman, J. Oxidant stress evoked by pacemaking in dopaminergic neurons is attenuated by DJ Hagenston, A. MGluR-mediated calcium waves that invade the soma regulate firing in layer V medial prefrontal cortical pyramidal neurons. Cortex 18, — Hagler, D.

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Properties of synchronous and asynchronous release during pulse train depression in cultured hippocampal neurons. Hakamata, Y. Heeman, B. Depletion of PINK1 affects mitochondrial metabolism, calcium homeostasis and energy maintenance. Cell Sci. Herman, J. Aging 19, — Hertle, D. Distribution of inositol-1,4,5-trisphosphate receptor isotypes and ryanodine receptor isotypes during maturation of the rat hippocampus.

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