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Книги з теми "Neuronal signaling"

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Neuronal signaling.

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 29 січня 2023

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1

Hatton, Glenn I., and Vladimir Parpura, eds. Glial ⇔ Neuronal Signaling. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7937-5.

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2

Tasker, Jeffrey G., Jaideep S. Bains, and Julie A. Chowen, eds. Glial-Neuronal Signaling in Neuroendocrine Systems. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62383-8.

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3

Wen, Joseph Yao Min. Neuronal-glial signaling involved in explant induced satellite cell proliferation in the adult trigeminal ganglia. Ottawa: National Library of Canada, 1993.

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4

Ron, Wallace. Membrane microdomain regulation of neuron signaling. New York: Nova Science Publishers, 2008.

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5

Membrane microdomain regulation of neuron signaling. New York: Nova Science Publishers, 2008.

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6

Chadwick, Derek J., and Jamie Goode, eds. Purinergic Signalling in Neuron-Glia Interactions. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/9780470032244.

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7

Derek, Chadwick, Goode Jamie, Novartis Foundation, and Symposium on Purinergic Signalling in Neuron-Glia Interactions (2005 : London, England), eds. Purinergic signalling in neuron-glia interactions. Chichester: John Wiley & Sons, 2006.

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8

N, Verkhratskiĭ A., ed. Calcium signalling in the nervous system. Chichester: Wiley, 1995.

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9

W, Arbuthnott Gordon, and Emson P. C, eds. Chemical signalling in the basal ganglia. Amsterdam: Elsevier, 1993.

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10

L, Iversen Leslie, Goodman E. C, and Neuroscience Research Centre (Merck Sharp & Dohme), eds. Fast and slow chemical signalling in the nervous system. Oxford: Oxford University Press, 1986.

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11

1951-, Urban Laszlo, North Atlantic Treaty Organization. Scientific Affairs Division., and NATO Advanced Research Workshop on Cellular Mechanisms of Sensory Processing (1993 : Wye, England), eds. Cellular mechanisms of sensory processing: The somatosensory system. Berlin: Springer-Verlag, 1994.

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12

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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13

1934-, Hatton Glenn I., and Parpura Vladimir 1964-, eds. Glial neuronal signaling. Boston: Kluwer Academic Publishers, 2004.

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14

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

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15

Parpura, Vladimir, and Glenn I. Hatton. Glial ⇔ Neuronal Signaling. Springer London, Limited, 2004.

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16

(Editor), Glenn I. Hatton, and Vladimir Parpura (Editor), eds. Glial Neuronal Signaling (Falk Symposium). Springer, 2004.

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17

Brambilla, Riccardo, ed. Neuronal cell signaling and behavior. Frontiers Media SA, 2013. http://dx.doi.org/10.3389/978-2-88919-082-9.

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18

Bains, Jaideep S., Julie A. Chowen, and Jeffrey G. Tasker. Glial-Neuronal Signaling in Neuroendocrine Systems. Springer International Publishing AG, 2022.

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19

Bains, Jaideep S., Julie A. Chowen, and Jeffrey G. Tasker. Glial-Neuronal Signaling in Neuroendocrine Systems. Springer International Publishing AG, 2021.

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20

Yakura, Hidetaka. Kinases and Phosphatases in Lymphocyte and Neuronal Signaling. Springer, 1997.

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21

Wislet-Gendebien, Sabine, ed. Trends in Cell Signaling Pathways in Neuronal Fate Decision. InTech, 2013. http://dx.doi.org/10.5772/3445.

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22

Guido, Mario Eduardo, Gabriela Alejandra Salvador, and Alejandra Alonso, eds. Emerging Mechanisms in Neuronal Signaling: From Cell Biology to Pathogenesis. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-111-4.

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23

Fields, R. Douglas. Beyond the Synapse: Cell-Cell Signaling in Synaptic Plasticity. Cambridge University Press, 2012.

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24

Douglas, Fields R., ed. Beyond the synapse: Cell-cell signaling in synaptic plasticity. Cambridge: Cambridge University Press, 2008.

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25

Zilliox, Lindsay, and James W. Russell. Diabetic and Prediabetic Neuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0115.

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Анотація:

Impaired glucose regulation (IGR) constitutes a spectrum of impaired glucose and metabolic regulation that can result in neuropathy. Several different pathways of injury in the diabetic peripheral nervous system that include metabolic dysregulation induced by metabolic syndrome induce oxidative stress, failure of nitric oxide regulation, and dysfunction of certain key signaling pathways. Oxidative stress can directly injure both dorsal route ganglion neurons and axons. Modulation of the nitric oxide system may have detrimental effects on endothelial function and neuronal survival. Reactive oxidative species can alter mitochondrial function, protein and DNA structure, interfere with signaling pathways, and deplete antioxidant defenses. Advanced glycelation end (AGE) products and formation of ROS are activated by and in turn regulate key signal transduction pathways.

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26

McGaugh, James L., and Robert C. A. Frederickson. Peripheral Signaling of the Brain: Role in Neural-Immune Interactions and Learning and Memory (Neuronal Control of Bodily Function). Hogrefe & Huber Pub, 1990.

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27

Hinder, Lucy M., Kelli A. Sullivan, Stacey A. Sakowski, and Eva L. Feldman. Mechanisms Contributing to the Development and Progression of Diabetic Polyneuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0114.

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Анотація:

Advances in our understanding of diabetes in human patients and experimental models indicate that a number of mechanisms may contribute to sensory nerve damage in diabetic polyneuropathy (DPN). In addition to oxidative stress, hyperglycemia and hyperlipidemia, recent research in pain, advanced glycation endproduct (AGE), and proteomics specify a contributory role for altered neuronal calcium homeostasis in DPN. Technology advances indicate neuronal energy balance and mitochondrial biogenesis, fission, and fusion are additional potential mechanisms. The effects of dysregulation or loss of insulin signaling and the effects of glucagon-like peptide-1 (GLP-1) and its receptor (GLP-1R) are also implicated.

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28

Bradbury, Elizabeth J., and Nicholas D. James. Mapping of neurotrophin receptors on adult sensory neurons. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0022.

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The paper discussed in this chapter describes the first mapping of neurotrophin receptors in adult sensory neurons. Neurotrophins and their receptors were a particularly hot topic at the time, but the primary focus of interest had been in their role in development. In this paper, McMahon and colleagues characterized both mRNA and protein expression of the recently discovered trk receptors on defined populations of adult sensory neurons, correlating trk expression with other primary afferent projection neuron properties such as cell size and neuronal function. Furthermore, by showing clear correlations between the expression of different trk receptors and the physical and functional properties of defined primary afferent projections, the authors provided key evidence suggesting that nerve growth factor and neurotrophin-3 acted on functionally distinct populations of adult sensory neurons. This paper provided the basis for subsequent research on neurotrophin signalling and function in both the healthy and the diseased nervous system.

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29

McCracken, Lindsay M., Mandy L. McCracken, and R. Adron Harris. Mechanisms of Action of Different Drugs of Abuse. Edited by Kenneth J. Sher. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199381678.013.010.

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Drugs of abuse represent a spectrum of chemically diverse compounds that are used via various routes of drug administration depending on the drug and its preparation. Although the exact molecular mechanisms by which these agents act to produce their intoxicating effects are not completely understood, many drugs of abuse are known to bind to specific neuronal membrane proteins that produce effects on cellular signaling and ultimately on behavior. With repeated administration of a drug, individuals often develop tolerance, and discontinuation of drug use following chronic administration typically results in withdrawal symptoms. This chapter describes the mechanism of action for the following classes of drugs of abuse: alcohol, cannabinoids, hallucinogens, inhalants, nicotine, opioids, sedative hypnotics, and stimulants. In addition, mechanisms of tolerance and withdrawal are discussed.

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30

Tong, Qingchun. Neuron Signaling in Metabolic Regulation. Taylor & Francis Group, 2021.

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31

Tong, Qingchun. Neuron Signaling in Metabolic Regulation. Taylor & Francis Group, 2021.

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32

Tong, Qingchun. Neuron Signaling in Metabolic Regulation. Taylor & Francis Group, 2021.

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33

Tong, Qingchun. Neuron Signaling in Metabolic Regulation. Taylor & Francis Group, 2021.

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34

Vincent, Pierre, and Nicholas C. Spitzer, eds. Dynamics of cyclic nucleotide signaling in neurons. Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-646-3.

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35

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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Анотація:

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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36

Goode, Jamie A., and Derek J. Chadwick. Purinergic Signalling in Neuron-Glia Interactions. Wiley & Sons, Incorporated, John, 2006.

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37

Goode, Jamie A., and Derek J. Chadwick. Purinergic Signalling in Neuron-Glia Interactions. Wiley & Sons, Incorporated, John, 2009.

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38

Foundation, Novartis. Purinergic Signalling in Neuron-Glia Interactions (Novartis Foundation Symposia). Wiley, 2006.

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39

Kauffman, Alexander S., and Jeremy T. Smith. Kisspeptin Signaling in Reproductive Biology. Springer, 2013.

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40

Kauffman, Alexander S., and Jeremy T. Smith. Kisspeptin Signaling in Reproductive Biology. Springer, 2015.

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41

Kauffman, Alexander S., and Jeremy T. Smith. Kisspeptin Signaling in Reproductive Biology. Springer London, Limited, 2013.

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42

Beninger, Richard J. Mechanisms of dopamine-mediated incentive learning. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0012.

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Mechanisms of dopamine-mediated incentive learning explains how sensory events, resulting from an animal’s movement and the environment, activate cortical glutamatergic projections to dendritic spines of striatal medium spiny neurons to initiate a wave of phosphorylation. If no rewarding stimulus is encountered, a subsequent wave of phosphatase activity undoes the phosphorylation. If a rewarding stimulus is encountered, dopamine initiates a cascade of events in D1 receptor-expressing medium spiny neurons that may prevent the phosphatase effects and work synergistically with signaling events produced by glutamate. As a result, corticostriatal synapses have a greater impact on response systems; this may be part of the mechanism of incentive learning. Dopamine acting on dendritic spines of D2 receptor-expressing medium spiny neurons may prevent synaptic strengthening by inhibiting adenosine signaling; these synapses may be weakened through mechanisms involving endocannabinoids. When dopamine concentrations drop, e.g. during negative prediction errors, the opposite may occur, producing inverse incentive learning.

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43

Foundation, Novartis. Purinergic Signalling in Neuron-glia Interactions, No. 276 (Novartis Foundation Symposium). John Wiley and Sons Ltd, 2006.

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44

Signaling at the synapse: Review supplement to Cell volume 72/Neuron volume 10. Cambridge, Mass: Cell Press, 1993.

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45

M, Jessell Thomas, ed. Signaling at the synapse: Review supplement to Cell volume 72/Neuron volume 10. Cambridge, Mass: Cell Press, 1993.

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46

Beninger, Richard J. Drug abuse and incentive learning. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0010.

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Анотація:

Drug abuse and incentive learning explains how abused drugs, including nicotine, ethanol, marijuana, amphetamine, cocaine, morphine, and heroin, produce conditioned place preference and are self-administered; dopamine receptor antagonists block these effects. Stimuli that become reliable predictors of drug reward produce burst firing in dopaminergic neurons, but the drug retains its ability to activate dopaminergic neurons. Thus, repeated drug users experience two activations of dopaminergic neurotransmission, one upon exposure to the conditioned stimuli signaling the drug and another upon taking the drug. This may lead to long-term neurobiological changes that contribute to withdrawal and addiction. Withdrawal can be remediated by abstinence but this does not reduce the conditioned incentive value of cues associated with drug taking; those cues can lead to relapse. Effective treatment will include detoxification and systematic exposure to drug taking-associated conditioned incentive stimuli in the absence of drug so that those stimuli lose their ability to control responses.

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47

New York Academy of Sciences Staff (Contributor) and Marc Diederich (Editor), eds. Signal Transduction Path Part D: Stress Signaling and Transcriptional Control (Annals of the New York Academy of Sciences). Blackwell Publishing Limited, 2007.

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48

Mira, Helena, Aixa Victoria Morales, and Ruth Diez Del Corral, eds. Generation of Neurons and Their Integration in Pre-Existing Circuits in the Postnatal Brain: Signalling in Physiological and Regenerative Contexts. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-988-5.

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49

Weiner, Howard, and Peter B. Crino. Familial tumour syndromes: tuberous sclerosis complex. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0017.

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Анотація:

Tuberous sclerosis complex (TSC) is a multisystem, genetic disorder that results from mutations in TSC1 or TSC2 genes. Neurological and neuropsychiatric disabilities include epilepsy, intellectual disability, autism, attention deficit disorder, and generalized anxiety. Cortical dysplasias (also known as tubers) are developmental abnormalities of the cerebral cortex that are believed to be responsible for seizures, cognitive disability, and autism. Subependymal giant cell astrocytomas (SEGAs) are intraventricular tumours that can cause hydrocephalus, increased intracranial pressure, and death. TSC results from hyperactivation of the mammalian target of rapamycin (mTOR) pathway in neurons in the brain. This chapter reviews the clinical presentations of TSC as well as diagnostic approaches for epilepsy and SEGAs. It discusses the genetics and cellular pathogenesis of TSC as well as reviewing the link to mTOR signalling. This chapter also presents evidence for different treatment modalities for seizures and SEGAs. It is written for qualified specialist physicians and caregivers.

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50

Urban, Laszlo. Cellular Mechanisms of Sensory Processing: The Somatosensory System (Nato a S I Series Series H, Cell Biology). Springer-Verlag Telos, 1994.

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