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Books on the topic 'Neuronal cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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1

Amini, Shohreh, and Martyn K. White. Neuronal cell culture: Methods and protocols. New York: Humana Press, 2013.

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2

Kempermann, Gerd. Adult neurogenesis: Stem cells and neuronal development in the adult brain. New York, NY: Oxford University Press, 2006.

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3

Adult neurogenesis: Stem cells and neuronal development in the adult brain. New York: Oxford University Press, 2005.

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4

Ulrich, Henning. Perspectives of Stem Cells: From tools for studying mechanisms of neuronal differentiation towards therapy. Dordrecht: Springer Science+Business Media B.V., 2010.

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5

Carter, Sylvia M. A comparative study of Rohon-Beard cells and associated neuronal components in fish and amphibian larvae. Portsmouth: Portsmouth Polytechnic, 1991.

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6

Plasticity in nerve cell function. Oxford: Clarendon Press, 1998.

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7

Schmid, Carl J., and Jason L. Wolfe. Neuronal cell apoptosis. Hauppauge, N.Y: Nova Science Publisher's, 2011.

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8

Lossi, Laura, and Adalberto Merighi, eds. Neuronal Cell Death. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2152-2.

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9

Amini, Shohreh, and Martyn K. White, eds. Neuronal Cell Culture. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-640-5.

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10

Amini, Shohreh, and Martyn K. White, eds. Neuronal Cell Culture. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1437-2.

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11

Herrera, Esperanza Meléndez, Bryan V. Phillips-Farfán, and Gabriel Gutiérrez Ospina. Endothelial cell plasticity in the normal and injured central nervous system. Boca Raton: CRC Press/Taylor & Francis, 2015.

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12

Copani, Agata, and F. Nicoletti. Cell-cycle mechanisms and neuronal cell death. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2005.

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13

Copani, Agata, and Ferdinando Nicoletti, eds. Cell-Cycle Mechanisms and Neuronal Cell Death. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-29390-6.

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14

Jitka, Ourednick, ed. Stem cell biology: Development and plasticity. New York, N.Y: New York Academy of Sciences, 2005.

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15

Nerve cells and animal behaviour. Cambridge: Cambridge University Press, 1989.

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16

Merighi, Adalberto, and Laura Lossi. Neuronal cell death: Methods and protocols. New York: Humana Press, 2015.

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17

K, Kaczmarek Leonard, ed. The neuron: Cell and molecular biology. 3rd ed. Oxford: Oxford University Press, 2002.

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18

Levitan, Irwin B. The neuron: Cell and molecular biology. 2nd ed. New York: Oxford University Press, 1997.

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19

Levitan, Irwin B. The neuron: Cell and molecular biology. New York: Oxford University Press, 1991.

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20

Bloom, Ona. Cells of the nervous system. Philadelphia: Chelsea House Publishers, 2005.

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21

Berry, M. The nerve cell. London: Mac Keith Press in association with Blackwell Scientific Pub., Oxford ; J.P. Lippincott Co., Philadelphia, Pa., 1986.

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22

Paolo, Zatta, and Nicolini Marino, eds. Non-neuronal cells in Alzheimer's disease. Singapore: World Scientific, 1995.

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23

Zatta, P., and M. Nicolini. Non-Neuronal Cells in Alzheimer's Disease. WORLD SCIENTIFIC, 1995. http://dx.doi.org/10.1142/2596.

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24

Tremblay, Marie-Ève, ed. Non-Neuronal Cells Editor’s Pick 2021. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-958-5.

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25

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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26

E, Rodriguez-Boulan, Nelson W. J, and Keystone Meeting on Epithelial and Nueronal Cell Polarity and Differentiation (1993 : Tamarron, Colo.), eds. Epithelial and neuronal cell polarity and differentiation. Cambridge [England]: Company of Biologists Ltd., 1993.

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27

1935-, Jacklet Jon W., ed. Neuronal and cellular oscillators. New York: Marcel Dekker, 1989.

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28

Nat, Roxana, and Andreas Eigentler. Cell Culture, iPS Cells and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0013.

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Somatic reprogramming technology, which enables the conversion of adult human non-neural cells into neurons, has progressed rapidly in recent years. The derivation of patient-specific induced pluripotent stem (iPS) cells has become routine. The inherent broad differentiation potential of iPS cells makes possible the generation of diverse types of human neurons. This constitutes a remarkable step in facilitating the development of more appropriate and comprehensive preclinical human disease models, as well as for high throughput drug screenings and cell therapy. This chapter reviews recent progress in the human iPS cell culture models related to common and rare NDDs, such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, spinal muscular atrophy, and degenerative ataxias. It focuses on the pathophysiological features revealed in cell cultures, and the neuronal subtypes most affected in NDDs. The chapter discusses the validity, limitation, and improvements of this system in faithfully and reproducibly recapitulating disease pathology.
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29

Non-Neuronal Cells of the Nervous System: Function and Dysfunction. Elsevier, 2003. http://dx.doi.org/10.1016/s1569-2558(00)x9001-7.

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30

Gottlieb, Jacqueline. Neuronal Mechanisms of Attentional Control. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.033.

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Damage to the human inferior parietal lobe produces an attentional disturbance known as contralateral neglect, and neurophysiological studies in monkeys have begun to unravel the cellular basis of this function. Converging evidence suggests that LIP encodes a sparse topographic map of the visual world that highlights attention-worthy objects or locations. LIP cells may facilitate sensory attentional modulations, and ultimately the transient improvement in perceptual thresholds that is the behavioural signature of visual attention. In addition, LIP projects to oculomotor centres where it can prime the production of a rapid eye movement (saccade). Importantly, LIP cells can select visual targets without triggering saccades, showing that they implement an internal (covert) form of selection that can be flexibly linked with action by virtue of additional, independent mechanisms. The target selection response in LIP is modulated by bottom-up factors and by multiple task-related factors. These modulations are likely to arise through learning and may reflect a multitude of computations through which the brain decides when and to what to attend.
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31

Jef ferys, John G. R. Cortical activity: single cell, cell assemblages, and networks. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0004.

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This chapter describes how the activity of neurons produces electrical potentials that can be recorded at the levels of single cells, small groups of neurons, and larger neuronal networks. It outlines how the movement of ions across neuronal membranes produces action potentials and synaptic potentials. It considers how the spatial arrangement of specific ion channels on the neuronal surface can produce potentials that can be recorded from the extracellular space. Finally, it outlines how the layered cellular structure of the neocortex can result in summation of signals from many neurons to be large enough to record through the scalp as evoked potentials or the electroencephalogram.
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32

Ischemia in neuronal PC12 cells: Role of free radical generation and cellular damage. Ottawa: National Library of Canada, 2001.

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33

Cohen, Marlene R., and John H. R. Maunsell. Neuronal Mechanisms of Spatial Attention in Visual Cerebral Cortex. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.007.

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Attention is associated with improved performance on perceptual tasks and changes in the way that neurons in the visual system respond to sensory stimuli. While we now have a greater understanding of the way different behavioural and stimulus conditions modulate the responses of neurons in different cortical areas, it has proven difficult to identify the neuronal mechanisms responsible for these changes and establish a strong link between attention-related modulation of sensory responses and changes in perception. Recent conceptual and technological advances have enabled progress and hold promise for the future. This chapter focuses on newly established links between attention-related modulation of visual responses and bottom-up sensory processing, how attention relates to interactions between neurons, insights from simultaneous recordings from groups of cells, and how this knowledge might lead to greater understanding of the link between the effects of attention on sensory neurons and perception.
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34

Seth, Rohit. Zinc deficiency induces apoptosis via mitochondrial p53- and caspase-dependent pathways in human neuronal precursor cells. Elseveir, 2014.

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35

Rolfs, A. Isolation and Induction of Neuronal Progenitor Cells: Rostock Spring School 2006 Contributions, Special Issue, Neurodegenerative Diseases 2007. S Karger Pub, 2007.

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36

Wainger, Brian J. Amyotrophic Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0028.

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Mouse and cellular models of ALS including stem cells have revealed tremendous insight into the molecular processes that lead to ALS. Models of ALS and other neurodegenerative diseases have led to emergent molecular themes that span several diseases. Future models must account for neuronal subtype specificity of different neurodegenerative diseases, particularly between tightly related diseases such as FTD and ALS. Human iPSC-derived motor neurons offer promise both with regard to the use of human cells and in particular the ability to model sporadic disease, which is critically important given the overwhelming abundance of sporadic disease in ALS and other neurodegenerative diseases.
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37

The role of f G[alpha]o and G[alpha]s isoforms in neuronal development: Studies in PC12 cells. Ottawa: National Library of Canada, 1994.

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38

Roy, Deboleena. The effects of melatonin and gonadal steroids on gonadotropin-releasing hormone (GnRH)regulation in hypothalamic GT1-7 neuronal cells. 2001.

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39

Byrne, John H., ed. The Oxford Handbook of Invertebrate Neurobiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190456757.001.0001.

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Invertebrates have proven to be extremely useful models for gaining insights into the neural and molecular mechanisms of sensory processing, motor control, and higher functions, such as feeding behavior, learning and memory, navigation, and social behavior. Their enormous contribution to neuroscience is due, in part, to the relative simplicity of invertebrate nervous systems and, in part, to the large cells found in some invertebrates, like mollusks. Because of the organizms’ cell size, individual neurons can be surgically removed and assayed for expression of membrane channels, levels of second messengers, protein phosphorylation, and RNA and protein synthesis. Moreover, peptides and nucleotides can be injected into individual neurons. Other invertebrate systems such as Drosophila and Caenorhabditis elegans are ideal models for genetic approaches to the exploration of neuronal function and the neuronal bases of behavior. The Oxford Handbook of Invertebrate Neurobiology reviews neurobiological phenomena, including motor pattern generation, mechanisms of synaptic transmission, and learning and memory, as well as circadian rhythms, development, regeneration, and reproduction. Species-specific behaviors are covered in chapters on the control of swimming in annelids, crustacea, and mollusks; locomotion in hexapods; and camouflage in cephalopods. A unique feature of the handbook is the coverage of social behavior and intentionality in invertebrates. These developments are contextualized in a chapter summarizing past contributions of invertebrate research as well as areas for future studies that will continue to advance the field.
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40

Koch, Christof. Biophysics of Computation. Oxford University Press, 1998. http://dx.doi.org/10.1093/oso/9780195104912.001.0001.

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Neural network research often builds on the fiction that neurons are simple linear threshold units, completely neglecting the highly dynamic and complex nature of synapses, dendrites, and voltage-dependent ionic currents. Biophysics of Computation: Information Processing in Single Neurons challenges this notion, using richly detailed experimental and theoretical findings from cellular biophysics to explain the repertoire of computational functions available to single neurons. The author shows how individual nerve cells can multiply, integrate, or delay synaptic inputs and how information can be encoded in the voltage across the membrane, in the intracellular calcium concentration, or in the timing of individual spikes. Key topics covered include the linear cable equation; cable theory as applied to passive dendritic trees and dendritic spines; chemical and electrical synapses and how to treat them from a computational point of view; nonlinear interactions of synaptic input in passive and active dendritic trees; the Hodgkin-Huxley model of action potential generation and propagation; phase space analysis; linking stochastic ionic channels to membrane-dependent currents; calcium and potassium currents and their role in information processing; the role of diffusion, buffering and binding of calcium, and other messenger systems in information processing and storage; short- and long-term models of synaptic plasticity; simplified models of single cells; stochastic aspects of neuronal firing; the nature of the neuronal code; and unconventional models of sub-cellular computation. Biophysics of Computation: Information Processing in Single Neurons serves as an ideal text for advanced undergraduate and graduate courses in cellular biophysics, computational neuroscience, and neural networks, and will appeal to students and professionals in neuroscience, electrical and computer engineering, and physics.
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41

Lees, A. J. Parkinson’s disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0008.

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The following landmark discoveries in our understanding of Parkinson’s disease are considered in this chapter: the first full medical description of the malady; consistent severe loss of pigmented cells in the substantia nigra; severe depletion of striatal dopamine; the use of high doses of racemic dopa to improve the motor symptoms; a superior animal model for the study of potential new treatments; functional lesioning and deep brain stimulation to relieve symptoms; capability of fetal dopamine cells to reinnervate the striatum and improve handicap; a compensatory phase before the emergence of motor symptoms and nigral cell loss beginning about five years prior to the onset of presenting symptoms; a large autosomal dominant family with Parkinsonism found to carry a genetic mutation of alpha synuclein; and discovery of Lewy bodies in surviving grafted fetal neuronal cells many years after successful implantation.
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42

Hertz, L. Non-Neuronal Cells of the Nervous System: Function and Dysfunction: Part I: Structure, Organization, Development and Regeneration
Part II: Biochemistry, ... (Advances in Molecular and Cell Biology). 3rd ed. Elsevier Science, 2003.

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43

Levitan, Irwin B., and Leonard K. Kaczmarek. The Neuron. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199773893.001.0001.

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The Fourth Edition of The Neuron provides a comprehensive first course in the cell and molecular biology of nerve cells. It begins with properties of the many newly discovered ion channels that have emerged through mapping of the genome and which shape the way a single neuron generates varied patterns of electrical activity. It also covers the molecular mechanisms that convert electrical activity into the secretion of neurotransmitter hormones at synaptic junctions between neurons. It discusses the biochemical pathways that are linked to the action of neurotransmitters and that can alter the cellular properties of neurons or sensory cells that transduce information from the outside world into the electrical code used by neurons, and the rapidly expanding knowledge of the molecular factors that induce an undifferentiated cell to become a neuron, and then guide it to form appropriate synaptic connections with its partners. Also addressed is the role of ongoing experience and activity in shaping these connections, and the mechanisms thought to underlie the phenomena of learning and memory.
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44

Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.

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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.
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45

Shandling, Relif J. Neuronal Cell Apoptosis Research. Nova Science Publishers, 2007.

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46

Shandling, Relif J. Neuronal Cell Apoptosis Research. Nova Science Publishers Inc, 2006.

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47

Shandling, Relif J. Neuronal Cell Apoptosis Research. Nova Science Publishers Inc, 2006.

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48

Cummings, Jeffrey L., and Jagan A. Pillai. Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0001.

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Neurodegenerative diseases (NDDs) are growing in frequency and represent a major threat to public health. Advances in scientific progress have made it clear that NDDs share many underlying processes, including shared intracellular mechanisms such as protein misfolding and aggregation, cell-to-cell prion-like spread, growth factor signaling abnormalities, RNA and DNA disturbances, glial cell changes, and neuronal loss. Transmitter deficits are shared across many types of disorders. Means of studying NDDs with human iPS cells and transgenic models are similar. The progression of NDDs through asymptomatic, prodromal, and manifest stages is shared across disorders. Clinical features of NDDs, including cognitive impairment, disease progression, age-related effects, terminal stages, neuropsychiatric manifestations, and functional disorders and disability, have many common elements. Clinical trials, biomarkers, brain imaging, and regulatory aspects of NDD can share information across NDDs. Disease-modifying and transmitter-based therapeutic interventions, clinical trials, and regulatory approaches to treatments for NDDs are also similar.
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49

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 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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50

Parpura, Vladimir, and Glenn I. Hatton. Glial ⇔ Neuronal Signaling. Springer, 2012.

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