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Data publikacji: 6 lipca 2024

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1

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

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2

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

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3

J, Bean Andrew, red. Protein trafficking in neurons. Amsterdam: Elsevier/Academic Press, 2007.

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4

Wiley, Ronald G. Suicide transport and immunolesioning. Austin: R.G. Landes, 1994.

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5

Veli, Himanen, Nijkamp Peter, Reggiani Aura i Raitio Juha, red. Neural networks in transport applications. Aldershot, Hants, England: Ashgate, 1998.

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6

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

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7

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

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8

1953-, Iverson Linda E., Conn P. Michael i Rudy Bernardo, red. Ion channels. San Diego: Academic Press, 1992.

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9

Cytoskeleton of the nervous system. New York: Springer, 2011.

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10

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

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11

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

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12

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

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13

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

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14

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

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15

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

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16

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 soma to synaptic terminals is required. Glial cells wrap axons in myelin, which speeds up information transfer. Axonal transport is necessary to maintain neuronal function and health across the long distances separating synaptic terminals and somata. A common mechanism of neurodegeneration arises from impairments in axonal transport that lead to protein aggregation and neuronal death.

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17

Sada, Nagisa, i Tsuyoshi Inoue. Lactate Dehydrogenase. Redaktor 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 shuttle, and its inhibition hyperpolarizes neurons and suppresses seizures. This enzyme is also a molecular target of stiripentol, a clinically used antiepileptic drug for Dravet syndrome. This review provides an overview of electrical regulation by the astrocyte-neuron lactate shuttle, and then introduces LDH as a metabolic target against epilepsy.

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18

Zuccato, Chiara, i 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 adult brain, HTT acts as an antiapoptotic protein and promotes transcription of neuronal genes and vesicle transport. Subversion or exacerbation of HTT brain function by an abnormally expanded polyQ repeat contributes to neuronal vulnerability in HD and suggests that loss of normal HTT function may be implicated in the disease.

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19

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

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20

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

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21

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

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22

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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23

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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24

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

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25

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

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26

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

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27

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

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28

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

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29

Gaitanis, John, Phillip L. Pearl i Howard Goodkin. The EEG in Degenerative Disorders of the Central Nervous System. Redaktorzy Donald L. Schomer i 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 energy metabolism (mitochondrial disorders, glucose transporter defect), neuronal toxicity (amino and organic acidopathies), impaired neuronal function (lysosomal and peroxisomal disorders), alteration of neurotransmitter systems (nonketotic hyperglycinemia), and vitamin and co-factor dependency (pyridoxine-dependent seizures). Environmental causes of perinatal brain injury often result in motor or intellectual impairment (cerebral palsy). Multiple proposed etiologies exist for autism, many focusing on synaptic development. This chapter reviews the EEG findings associated with this myriad of pathologies occurring in childhood.

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30

(Editor), Abel Lajtha, i Maarten E.A. Reith (Editor), red. Handbook of Neurochemistry and Molecular Neurobiology: Neural Membranes and Transport (Springer Reference). Wyd. 3. Springer, 2007.

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31

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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32

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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33

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 in the patient on neuroleptic therapy that cannot be stopped who has developed parkinsonism. Dopamine transporter imaging should be normal in drug-induced tremor.

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34

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

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35

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

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36

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

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37

Shaw, Pamela, i 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. However, partial involvement of the trigeminal nerve, particularly the sensory component, is relatively common, the main symptoms being numbness and pain. Reactivation of herpes zoster in the trigeminal nerve (shingles) can cause pain and a rash. Trigeminal neuralgia and sensory neuropathy are also discussed.Other disorders of the lower cranial nerves include Bell’s palsy, hemifacial spasm and glossopharyngeal neuralgia. Cavernous sinus, Tolosa–Hunt syndrome, jugular foramen syndrome and polyneuritis cranialis are caused by the involvement of more than one lower cranial nerve.Difficulty in swallowing, or dysphagia, is a common neurological problem and the most important consequences include aspiration and malnutrition (Wiles 1991). The process of swallowing is a complex neuromuscular activity, which allows the safe transport of material from the mouth to the stomach for digestion, without compromising the airway. It involves the synergistic action of at least 32 pairs of muscles and depends on the integrity of sensory and motor pathways of several cranial nerves; V, VII, IX, X, and XII. In neurological practice dysphagia is most often seen in association with other, obvious, neurological problems. Apart from in oculopharyngeal muscular dystrophy, it is relatively rare as a sole presenting symptom although occasionally this is seen in motor neurone disease, myasthenia gravis, and inclusion body myositis. Conversely, in general medical practice, there are many mechanical or structural disorders which may have dysphagia as the presenting feature. In some of the disorders, notably motor neurone disease, both upper and lower motor neurone dysfunction may contribute to the dysphagia. Once dysphagia has been identified as a real or potential problem, the patient should undergo expert evaluation by a clinician and a speech therapist, prior to any attempt at feeding. Videofluoroscopy may be required. If there is any doubt it is best to achieve adequate nutrition through the use of a fine-bore nasogastric tube and to periodically reassess swallowing. Anticholinergic drugs may be helpful to reduce problems with excess saliva and drooling that occur in patients with neurological dysphagia, and a portable suction apparatus may be helpful. Difficulty in clearing secretions from the throat may be helped by the administration of a mucolytic agent such as carbocisteine or provision of a cough assist device.

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38

1937-, Moss Stephen John, i Henley Jeremy, red. Receptor and ion-channel trafficking: Cell biology of ligand-gated and voltage-sensitive ion channels (molecular and cellular neurobiology). Oxford: Oxford University Press, 2002.

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39

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

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