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Books on the topic 'Transport neuronal'

Author: Grafiati

Published: 6 July 2024

Last updated: 31 July 2025

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1

Gribkoff, Valentin K. Structure, function, and modulation of neuronal voltage-gated ion channels. Wiley, 2009.

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2

1955-, Gonzalez-Lima Francisco, ed. Cytochrome oxidase in neuronal metabolism and Alzheimer's disease. Plenum Press, 1998.

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3

Veli, Himanen, Nijkamp Peter, Reggiani Aura, and Raitio Juha, eds. Neural networks in transport applications. Ashgate, 1998.

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4

A, Lappi Douglas, ed. Suicide transport and immunolesioning. R.G. Landes, 1994.

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5

Murdoch, Ritchie J., Keynes R. D, and Bolis Liana, eds. Ion channels in neural membranes: Proceedings of the 11th International Conference on Biological Membranes held at Crans-sur-Sierre, Switzerland, June 10-14, 1985. A.R. Liss, 1986.

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6

J, Alvarez-Leefmans F., Russell John M. 1942-, and International Brain Research Organization. Congress, eds. Chloride channels and carriers in nerve, muscle, and glial cells. Plenum Press, 1990.

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7

Suter, Daniel M., and Kyle E. Miller, eds. Neuronal Mechanics and Transport. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-823-8.

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8

Neuronal cytoskeleton: Morphogenesis, transport and synaptic transmission. Japan Scientific Societies Press, 1993.

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9

Elam, John. Axonal Transport in Neuronal Growth and Regeneration. Springer, 2013.

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10

Elam, John. Axonal Transport in Neuronal Growth and Regeneration. Springer London, Limited, 2013.

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11

Gonzalez-Lima, Francisco. Cytochrome Oxidase in Neuronal Metabolism and Alzheimer's Disease. Springer London, Limited, 2013.

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12

Mason, Peggy. Cells of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0002.

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The nervous system is made up of neurons and glia that derive from neuroectoderm. Since neurons are terminally differentiated and do not divide, primary intracranial tumors do not arise from mature neurons. Tumors outside the nervous system may metastasize inside the brain or may release a substance that negatively affects brain function, termed paraneoplastic disease. Neurons receive information through synaptic inputs onto dendrites and soma and send information to other cells via a synaptic terminal. Most neurons send information to faraway locations and for this, an axon that connects the

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13

Hirokawa, Nobutaka. Neuronal Cytoskeleton: Morphogenesis, Transport, and Synaptic Transmission (Taniguchi Symposia on Brain Sciences, No 16). CRC, 1994.

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14

Sada, Nagisa, and Tsuyoshi Inoue. Lactate Dehydrogenase. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0029.

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Glucose is transported into neurons and used as an energy source. It is also transported into astrocytes, a type of glial cell, and converted to lactate, which is then released to neurons and used as another energy source. The latter is called the astrocyte-neuron lactate shuttle. Although the lactate shuttle is a metabolic pathway, it also plays important roles in neuronal activities and brain functions. We recently reported that this metabolic pathway is involved in the antiepileptic effects of the ketogenic diet. Lactate dehydrogenase (LDH) is a metabolic enzyme that mediates the lactate sh

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15

Zuccato, Chiara, and Elena Cattaneo. Normal Function of Huntingtin. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0011.

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Huntingtin (HTT) is the 3,144–amino acid protein product of the Huntington’s disease gene (HTT), which can be traced back through 800 million years of evolution. It carries a trinucleotide CAG repeat that encodes polyglutamine (polyQ) at an evolutionarily conserved NH2-terminal position in exon 1. This chapter discusses the discoveries that have mapped the evolutionary history of HTT and the CAG repeat and the critical role of the protein in development as well as its activities in the adult brain. During embryogenesis, HTT is critical for gastrulation, neurulation, and neurogenesis. In the ad

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16

Protein Trafficking in Neurons. Academic Press, 2006.

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17

Bean, Andrew J. Protein Trafficking in Neurons. Elsevier Science & Technology Books, 2006.

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18

Sotnikov, O. S. Properties Live Axoplasm. Nova Science Publishers, Incorporated, 2015.

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19

Baumann, Pierre. Transport Mechanisms of Tryptophan in Blood Cells, Nerve Cells, and at the Blood-Brain Barrier: Proceedings of the International Symposium, Prilly/Lausanne, Switzerland, July 6-7 1978. Springer, 2013.

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20

Baumann, Pierre. Transport Mechanisms of Tryptophan in Blood Cells, Nerve Cells, and at the Blood-Brain Barrier: Proceedings of the International Symposium, ... of Neural Transmission. Supplementa ). Springer, 2014.

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21

Mutations in dynein link motor neuron degeneration to defects in retrograde transport. 2003.

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22

Breisgau, Universität Freiburg im, ed. Zielgene und retrograder Transport des Transkriptionsfaktors NF-kB [NF-KappaB]: Untersuchung der neuronalen Genexpression. 1999.

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23

Neural Networks in Transport Applications. Taylor & Francis Group, 2019.

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24

Reggiani, Aura, Peter Nijkamp, and Veli Himanen. Neural Networks in Transport Applications. Taylor & Francis Group, 2019.

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25

Reggiani, Aura, Peter Nijkamp, and Veli Himanen. Neural Networks in Transport Applications. Taylor & Francis Group, 2019.

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26

Reggiani, Aura, Peter Nijkamp, and Veli Himanen. Neural Networks in Transport Applications. Taylor & Francis Group, 2019.

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27

Gaitanis, John, Phillip L. Pearl, and Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0013.

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Nervous system alterations can occur at any stage of prenatal or postnatal development. Any of these derangements, whether environmental or genetic, will affect electrical transmission, causing electroencephalogram (EEG) alteration and possibly epilepsy. Genetic insults may be multisystemic (for example, neurocutaneous syndromes) or affect only the brain. Gene mutations account for inborn errors of metabolism, channelopathies, brain malformations, and impaired synaptogenesis. Inborn errors of metabolism cause seizures and EEG abnormalities through a variety of mechanisms, including disrupted e

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28

Kindler, Stefan. Klonierung der Mikrotubulus-assoziierten Proteine 2 der Ratte und Untersuchung des neuronalen mRNA-Transports. 1992.

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29

Eiki, Manami. Development of enteric serotonergic neurons: Role of transient extraganglionic 5-HT transport in phenotypic determination. 1998.

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30

Ion channels in neural membranes: Proceedings of the 11th International Conference on Biological Membranes held at Crans-sur-Sierre, Switzerland, June 10-14, 1985 (Neurology and neurobiology). A.R. Liss, 1986.

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31

Kirilly, Eszter. TIME COURSE OF NEURONAL DAMAGE AND RECOVERY INDUCED BY MDMA: EXPRESSION AND DISTRIBUTION OF SEROTONIN TRANSPORTER IN THE RAT BRAIN. VDM Verlag Dr. Müller, 2010.

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32

Walsh, Richard A. “I Am Not Sure If I Should Do DaT”. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0008.

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Nuclear medicine-based imaging techniques can provide an estimation of nigrostriatal tract denervation based on radionucleotide uptake in the distal presynaptic terminals of dopaminergic neurons. Although unhelpful in differentiating between differing etiologies of denervation in varied neurodegenerative disorders associated with parkinsonism, this imaging is justified in situations in which parkinsonism is believed to be drug-induced or functional or in cases in which subclinical parkinsonism is suspected. The most common clinical situation in which dopamine transporter imaging is helpful is

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33

Alvarez-Leefmans, F. J., and Russell John M. Chloride Channels and Carriers in Nerve, Muscle, and Glial Cells. Springer London, Limited, 2013.

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34

(Editor), John N. Abelson, Melvin I. Simon (Editor), Bernardo Rudy (Editor), and Linda E. Iverson (Editor), eds. Ion Channels, Volume 207 (Methods in Enzymology). Academic Press, 1992.

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35

Nixon, Ralph A., and Aidong Yuan. Cytoskeleton of the Nervous System. Springer, 2016.

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36

Shaw, Pamela, and David Hilton-Jones. The lower cranial nerves and dysphagia. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0429.

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Disorders affecting the lower cranial nerves – V (trigeminal), VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory) and XII (hypoglossal) – are discussed in the first part of this chapter. The clinical neuroanatomy of each nerve is described in detail, as are disorders – often in the form of lesions – for each nerve.Trigeminal nerve function may be affected by supranuclear, nuclear, or peripheral lesions. Because of the wide anatomical distribution of the components of the trigeminal nerve, complete interruption of both the motor and sensory parts is rarely observed in practice. Howe

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37

Stamer, Karsten. Untersuchung des Proteins Tau in der Maus-Neuroblastoma-Zellinie N2a (Olmsted et al., 1970) sowie in neuronalen Zellen aus der Ratte, Rattus norvegicus (Berkenhout, 1769) und der Maus, Mus musculus, Linné, 1758: Einfluss auf den Mikrotubuli-abhängigen Transport. 1999.

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38

(Editor), Stephen Moss, and Jeremy Henley (Editor), eds. Receptor and Ion-Channel Trafficking: Cell Biology of Ligand-Gated and Voltage Sensitive Ion Channels. Oxford University Press, USA, 2002.

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