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Books on the topic 'Neurones sensitifs'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 December 2024

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1

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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2

Sánchez Klinge, Marta Elena, and Claudia Aixa Mutis Barreto. Fisiología del sistema neuromuscular. Bogotá. Colombia: Universidad de La Salle. Ediciones Unisalle, 2013. http://dx.doi.org/10.19052/9789585148031.

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El sistema nervioso se encarga de recibir estímulos del exterior a través de los receptores sensoriales. Estos estímulos pueden ser de cualquier tipo, como los auditivos, visuales o táctiles. Muchos de los receptores están situados en toda la superficie del cuerpo. Luego de recibir los estímulos, los receptores que actúan como transductores (aquellos que transforma un tipo de energía en otra) los transforman en impulsos o potenciales de acción (PA) , conocidos también como excitaciones nerviosas que se dirigen hacia el sistema nervioso central (SNC) a través de los nervios periféricos de la vía aferente o neurona sensitiva. Dicho impulso se puede dirigir hacia diferentes segmentos del SNC como las áreas sensitivas de la médula espinal, la sustancia reticular, el cerebelo, el tálamo y las áreas somestésicas de la corteza cerebral.

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3

Liu, Shu. Temperature- and touch-sensitive neurons couple CNG and TRPV channel activities to control heat avoidance in Caenorhabditis elegans. Freiburg: Universität, 2012.

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4

P, Rauschecker Josef, and Marler Peter, eds. Imprinting and cortical plasticity: Comparative aspects of sensitive periods. New York: Wiley, 1987.

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5

Bilan musculaire et sensitif: Bases et techniques. Paris: Maloine, 2003.

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6

Urban, Laszlo. Cellular Mechanisms of Sensory Processing: The Somatosensory System. Springer London, Limited, 2013.

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7

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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8

Urban, Laszlo. Cellular Mechanisms of Sensory Processing: The Somatosensory System. Springer London, Limited, 2011.

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9

Pfäffle, Clara. Functional Imaging of Retinal Neurons: Phase-Sensitive Optical Coherence Tomography. Infinite Science Publishing, 2022.

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10

Frost, William, and Jian-young Wu. Voltage-Sensitive Dye Imaging. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199939800.003.0008.

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Voltage sensitive dye imaging (VSD) can be used to record neural activity in hundreds of locations in preparations ranging from mammalian cortex to invertebrate ganglia. Because fast VSDs respond to membrane potential changes with microsecond temporal resolution, these are better suited than calcium indicators for recording rapid neural signals. Here we describe methods for using a 464- element photodiode array and fast VSDs to record signals ranging from large scale network activity in brain slices and in vivo mammalian preparations, to action potentials in over 100 individual neurons in invertebrate ganglia.

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11

Martínez-François, Juan Ramón, Nika N. Danial, and Gary Yellen. Metabolic Seizure Resistance via BAD and KATP Channels. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0028.

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On a ketogenic diet, ketone bodies provide an alternative fuel, replacing much of the glucose used ordinarily by the brain. This switch is thought to underlie its anticonvulsant effects. Brain fuel utilization can also be modified by a nondietary approach: genetic alteration of the protein BAD, which has known roles in regulating both apoptosis and glucose metabolism. When the metabolic function of BAD is genetically altered in mice, it produces reduced glucose and increased ketone body metabolism in neurons and astrocytes. This effect is related to regulation of BAD by phosphorylation and is independent of its apoptotic function. Mice with BAD modifications that produce decreased glucose metabolism exhibit a marked increase in the activity of neuronal ATP-sensitive potassium (KATP) channels and strong resistance to behavioral and electrographic seizures in vivo. This seizure resistance is lost upon genetic ablation of KATP channels, suggesting that KATP channels mediate BAD’s anticonvulsant effect.

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12

Tamura, Connie S. Capsaicin-sensitive enteric neurons: Anatomy, function and role in the short-term control of food intake. 1995.

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13

Pharmacological agents against the neuronal voltage-sensitive calcium channels: Development of probes to characterize the cellular and molecular dynamics of neuronal calcium channels. Ottawa: National Library of Canada, 1994.

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14

Chubb, Charles, Joseph Darcy, Michael S. Landy, John Econopouly, Dan Bindman Jong-Ho Nam, and George Sperling. The Scramble Illusion. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199794607.003.0096.

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A “scramble” is a visual texture in which different gray levels are randomly mixed together. Past research has demonstrated that human vision has three dimensions of sensitivity to the different sorts of scrambles that can be created by varying the proportions of different gray levels included in the scramble. This chapter demonstrates two scrambles with dramatically different gray level histograms that appear identical unless the observer is specifically instructed to scrutinize each of them individually. It is argued that people fail to notice any difference between these two scrambles because there exist only three distinct classes of texture-sensitive neurons in the human brain that are differentially sensitive to scrambles, and in each of them these two scrambles produce identical levels of activation.

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15

de Carvalho, Mamede, and Michael Swash. Neurophysiology in amyotrophic lateral sclerosis and other motor degenerations. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199688395.003.0022.

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Electromyography is critical for the diagnosis of motor neuron disease, as its findings exclude mimicking disorders, and confirm signs of widespread motor unit loss and reinnervation. In chronic conditions the slow disease course allows giant, stable motor unit potentials to appear. In contrast, in amyotrophic lateral sclerosis, the rapid degenerative process is characterized by signs of denervation and unstable motor unit potentials, where motor units become dysfunctional before having time to sustain very large reinnervated motor unit potentials. Fasciculation potentials are observed in both conditions. In amyotrophic lateral sclerosis fasciculation potentials are important supporting electrodiagnostic evidence, permitting earlier diagnosis. Many methods have been developed to quantify and monitor the lower motor neuron pool, but few have been used in clinical trials. Their role as tools to follow interventions or to interpret pathogenesis remains incompletely explored. Electromyography is a sensitive and reliable test in the diagnosis and assessment of motor neuron diseases.

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16

Zhou, Juan, and William W. Seeley. Brain Circuits. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0007.

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Each neurodegenerative disease is defined by selectively vulnerable neurons, regions, networks, and functions, as well as genetic risk factors. In the past decade, new network-sensitive neuroimaging methods have made it possible to test the notion of network-based degeneration in living humans. This chapter focuses on two common causes of dementia, Alzheimer’s disease (AD) and frontotemporal dementia (FTD), but uses these diseases to illustrate class-wide neurodegeneration principles whenever possible. It first introduces two key concepts of neurodegenerative disease selective vulnerability: onset and progression. In parallel, it addresses two distinct but related observations about neurodegenerative disease: clinico-anatomical convergence and phenotypic heterogeneity. It then examines disease onset and models of progression in more detail, based on available neuroimaging evidence. Finally, it touches on the most important frontiers in the field of network-based neurodegeneration.

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17

(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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18

Price, Chane, Zahid Huq, Eellan Sivanesan, and Constantine Sarantopoulos. Pain Pathways and Pain Physiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190457006.003.0001.

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Pain is a multidimensional sensory experience that is mediated by complex peripheral and central neuroanatomical pathways and mechanisms. Typically, noxious stimuli activate specific peripheral nerve terminals onto Aδ‎ and C nerve fibers that convey pain and generate signals that are relayed and processed in the spinal cord and then conveyed via the spinothalamic tracts to the contralateral thalamus and from there to the brain. Acute pain is self-limited and resolves with the healing process, but conditions of extensive injury or inflammation sensitize the pain pathways and generate aberrant, augmented responses. Peripheral and central sensitization of neurons (as a result of spatially and temporally excessive inflammation or intense afferent signal traffic) may result in hyperexcitability and chronicity of pain, with spontaneous pain and abnormal evoked responses to stimuli (allodynia, hyperalgesia). Finally, neuropathic pain follows injury or disease to nerves as a result of hyperexcitability augmented by various sensitizing mechanisms.

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19

Passaro, Antony, Foteini Christidi, Vasiliki Tsirka, and Andrew C. Papanicolaou. White Matter Connectivity. Edited by Andrew C. Papanicolaou. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199764228.013.5.

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The applications of diffusion tensor imaging (DTI) have increased considerably among both normal and diverse neuropsychiatric populations in recent years. In this chapter, the authors examine the contributions of DTI in identifying profiles of trait-specific connectivity in several groups defined in terms of gender, age, handedness, and general intelligence. Additionally, the DTI literature is reviewed across a range of neurodegenerative disorders including Alzheimer’s disease, mild cognitive impairment, frontotemporal dementia, Parkinson disease, multiple sclerosis, and acquired neurological disorders resulting from neuronal injury such as traumatic brain injury, aphasia, agnosia, amnesia, and apraxia. DTI metrics sensitive to psychiatric disorders encompassing obsessive-compulsive disorder, depression, bipolar disorder, schizophrenia, and alcoholism are reviewed. Future uses of DTI as a promising means of confirming diagnoses and identifying in vivo early microstructural changes of patients’ clinical symptoms are discussed.

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20

Allen, Shelley J. Pathophysiology of Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0002.

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We now know that the onset of the pathological processes leading to Alzheimer’s disease (AD) may be 15–20 years before symptoms appear. This focuses attention on synaptic changes and the early role of tau, and less on the hallmark amyloid plaques (Aβ‎) and neurofibrillary tau tangles. Sensitive biomarkers to allow early screening will be essential. Familial autosomal AD is the result of mutations in one of three genes (APP, PSEN1, or PSEN2), each directly related to increased Aβ‎, and informs pathological mechanisms in common sporadic cases, but are also subject to influence by many risk genes and environmental factors. The essential role of apolipoprotein E in neuronal repair and Aβ‎ clearance provides a therapeutic target but also a challenge in carriers of the risk gene APOE4. Current treatments are symptomatic, derived from neurotransmitter deficits seen; particularly cholinergic, but emerging data suggest alternative targets which may prove more productive.

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21

Klein, Amanda H., and Matthias Ringkamp. Peripheral neural mechanisms of cutaneous heat hyperalgesia and heat pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0024.

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In the landmark paper discussed in this chapter, published in 1982, LaMotte et al. investigated the contribution of different cutaneous nerve fibres to heat pain and heat hyperalgesia in both psychophysical (humans) and electrophysiological studies (human and primates), using identical thermal test and conditioning stimuli; the findings from the two sets of experiments were then correlated. In non-human primates, neuronal activity was recorded from mechanoheat-sensitive A- and C-fibres (AMHs and CMHs, respectively) and warm and cold fibres, whereas, in conscious human volunteers, activity from CMHs was recorded. The authors found that pain is mediated by activity in CMHs and that sensitization of CMHs after a mild burn injury accounts for the increased heat pain after such injury. The combination of psychophysical experiments in human and correlative electrophysiological studies in non-human primates provides an important experimental approach for unravelling the contribution of different classes of afferents to pain.

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22

Lopes da Silva, Fernando H., and Eric Halgren. Neurocognitive Processes. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0048.

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Transmembrane neuronal currents that embody cognition in the cortex produce magnetoencephalographic and electroencephalographic signals. Frequency-domain analysis reveals standard rhythms with consistent topography, frequency, and cognitive correlates. Time-domain analysis reveals average event-related potentials and field (ERP/ERF) components with consistent topography, latency, and cognitive correlates. Standard rhythms and ERP/ERF components underlie perceiving stimuli; evaluating whether stimuli match predictions, and taking appropriate action when they do not; encoding stimuli to permit semantic processing and then accessing lexical representations and assigning syntactic roles; maintaining information in primary memory; preparing to take an action; and closing processing of an event–response sequence. Sustained mental processes are associated with theta and gamma. Consolidating memories appears to occur mainly during replay of specific firing patterns during sleep spindles and slow oscillations. Biophysical, neuroanatomical, and neurophysiological factors interact to render cognitive rhythms and components particularly sensitive to the large-scale modulatory processes that sequence and integrate higher cortical processing.

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23

Noebels, Jeffrey L., Massimo Avoli, Michael A. Rogawski, Annamaria Vezzani, and Antonio V. Delgado-Escueta, eds. Jasper's Basic Mechanisms of the Epilepsies. 5th ed. Oxford University PressNew York, 2024. http://dx.doi.org/10.1093/med/9780197549469.001.0001.

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Abstract Unverricht-Lundborg disease (ULD; EPM1) is an inherited neurodegenerative disorder characterized by onset at 6–15 years, stimulus-sensitive, action-activated myoclonus, epilepsy, and progressive neurological deterioration. It is caused by biallelic pathogenic variants in the CSTB gene, encoding a cystatin B. The most common of these is an unstable expansion of a dodecamer repeat element in the promoter region of the gene, leading to marked downregulation of CSTB expression. Total loss of CSTB is associated with severe neonatal-onset encephalopathy. A cystatin B–deficient mouse models the EPM1 disease relatively well. Myoclonic seizures, preceded by microglial activation, develop at one month of age and are followed by progressive gray and white matter degeneration and motor problems. CSTB is an inhibitor of cysteine proteases of the cathepsin family showing both nuclear and cytoplasmic localization with partial co-localization with lysosomal markers. CSTB function has been linked to protecting neurons from oxidative damage through an oxidative stress-responsive cystatin B-cathepsin B signaling pathway. In the nucleus CSTB has been shown to participate in regulation of cell cycle, and histone H3 tail proteolytic cleavage. Downstream effects of CSTB dysfunction have also been implicated in apopotosis, microglial dysfunction, inflammation, neurogenesis and synapse physiology. Despite the progress made, the exact disease mechanisms in EPM1 remain elusive. This chapter discusses the clinical features of EPM1 and recent advances in understanding its pathophysiology.

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