Books: 'Neuroni corticali'

1

N, Cooper Leon, ed. Theory of cortical plasticity. New Jersey: World Scientific, 2004.

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2

Neuronal Topography in a Cortical Circuit for Innate Odor Valence. [New York, N.Y.?]: [publisher not identified], 2020.

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3

Sam, Fazeli, and Collingridge G. L, eds. Cortical plasticity: LTP and LTD. Oxford: Bios Scientific, 1996.

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4

Ghai, Himesh S. Anoxia reduces whole cell permeability in cortical neurons of the anoxia tolerant turtle, Chrysemys picta belli. Ottawa: National Library of Canada, 1999.

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5

Coordinated activity in the brain: Measurements and relevance to brain function and behavior. Dordrecht: Springer, 2009.

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6

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

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7

Sattler, Rita. Effects of moderate and profound hypothermia on excitatory amino-acid-induced neuronal injury in cortical cell cultures. Ottawa: National Library of Canada, 1996.

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8

Żochowski, Michał. Synchrony in biological and physical systems: An experimental and theoretical study. Warszawa: Polska Akademia Nauk, Instytut Biocybernetyki i Inżynierii Biomedycznej, 2000.

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9

Gutnick, Michael J., and Istvan Mody, eds. The Cortical Neuron. Oxford University Press, 1995. http://dx.doi.org/10.1093/acprof:oso/9780195083309.001.0001.

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10

J, Gutnick M., and Mody Istvan 1957-, eds. The cortical neuron. New York: Oxford University Press, 1995.

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11

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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12

DeFelipe, Rockland, Javier, Kathleen S., ed. Cortical GABAergic neurons: stretching it. Frontiers Media SA, 2012. http://dx.doi.org/10.3389/978-2-88919-037-9.

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13

Bikoff, Jay Benjamin. Molecular mechanisms regulating cortical development: From neurons to synapses. 2007.

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14

The mouse mutant reeler causes increased adhesion in early postmitotic cortical neurons: Evidence for two separate neocortical neuronal lineages. Ottawa: National Library of Canada, 1995.

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15

Theory of cortical plasticity. Singapore: World Scientific, 2005.

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16

Meyer, Gundela. Genetic Control of Neuronal Migrations in Human Cortical Development. Springer London, Limited, 2007.

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17

Genetic Control of Neuronal Migrations in Human Cortical Development. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-36689-8.

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18

Shaibani, Aziz. Hyperreflexia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0018.

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Hyperactive deep tendon reflexes area sign of upper motor neuron lesion. They are also commonly seen in normal but tense people. Proper technique of reflexes examination and experience play a major role in eliciting and categorizing deep tendon reflexes. Clonus is the highest degree of hyperreflexia. The most important neuromuscular disease associated with hyperreflexia is ALS due to degeneration of the cortical motor neurons. Diagnostic difficulty occurs when hyperreflexia and spasticity are the only findings. In these cases, PLS, HSP, and other causes of myelopathies should be entertained. Jaw clonus often indicates a lesion above the midpontine level. When hyperreflexia is found, it is wise to look for other features of upper motor neuron dysfunction such as positive Babiniski signs and hypertonia.

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19

Traub, Roger D., John G. R. Jefferys, and Miles A. Whittington. Fast Oscillations in Cortical Circuits. MIT Press, 1999.

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20

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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21

Levine, Michael S., Elizabeth A. Wang, Jane Y. Chen, Carlos Cepeda, and Véronique M. André. Altered Neuronal Circuitry. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0010.

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In mouse models of Huntington’s disease (HD), synaptic alterations in the cerebral cortex and striatum are present before overt behavioral symptoms and cell death. Similarly, in HD patients, it is now widely accepted that early deficits can occur in the absence of neural atrophy or overt motor symptoms. In addition, hyperkinetic movements seen in early stages are followed by hypokinesis in the late stages, indicating that different processes may be affected. In mouse models, such behavioral alterations parallel complex biphasic changes in glutamate-mediated excitatory, γ‎-aminobutyric acid (GABA)-mediated inhibitory synaptic transmission and dopamine modulation in medium spiny neurons of the striatum as well as in cortical pyramidal neurons. The progressive electrophysiologic changes in synaptic communication that occur with disease stage in the cortical and basal ganglia circuits of HD mouse models strongly indicate that therapeutic interventions and strategies in human HD must be targeted to different mechanisms in each stage and to specific subclasses of neurons.

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22

Gong, Bo. Calcium-stimulated adenylyl cyclase 1 regulates synaptic scaling in forebrain cortical neurons. 2006.

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23

Ivanov, Tina Rhea. Gene expression in cortical neurons; analysis of the mouse 68kDA neurofilament gene. 1992.

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24

Fink, John K. Upper Motor Neuron Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0031.

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Symptomatic disturbance of corticospinal and corticobulbar tracts (collectively, the upper motor neuron UMN) occurs in innumerable acquired central nervous system disorders including the consequences of trauma, hypoxia-ischemia, inflammation (e.g. multiple sclerosis), toxins (e.g. thiocyanate1 and specific organophosphorus compound toxicity2) and deficiencies (e.g. hypocupremia3 and vitamin B12 deficiency). Variable degrees of UMN disturbance frequently accompany degenerative disorders in which disturbance of another neurologic system results in the primary clinical. Neuropathologic studies have shown prominent axon degeneration involving corticospinal tracts (HSP and PLS) and corticobulbar tracts (PLS); and mildly affecting dorsal columns (HSP and PLS to some degree). Myelin loss is considered secondary to axon degeneration. Loss of cortical motor neurons is observed in PLS. Anterior horn cells are typically spared in both HSP and PLS. Presently, treatment for HSP and PLS is symptomatic and includes physical therapy and spasticity reducing medications.

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25

Shaibani, Aziz. Hyperreflexia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0018.

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Hyperactive deep tendon reflexes (DTRs) is a sign of upper motor neuron (UMN) lesions. It is also commonly seen in normal but anxious people. The proper technique of deep tendon reflex examination and experience play a major role in eliciting and categorizing DTRs. Sustained clonus is the highest degree of hyperreflexia. The most important neuromuscular disease associated with hyperreflexia is amyotrophic lateral sclerosis (ALS) due to degeneration of the cortical motor neurons. Diagnostic difficulty occurs when hyperreflexia and spasticity are the only findings. In these cases, primary lateral sclerosis (PLS), hereditary spastic paraplegia (HSP), and other causes of myelopathies should be entertained. Compressive myelopathies are easily excludable by neuroimaging.

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26

Jones, Barbara E. Neuroanatomical, neurochemical, and neurophysiological bases of waking and sleeping. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0004.

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Neurons distributed through the reticular core of the brainstem, hypothalamus, and basal forebrain and giving rise to ascending projections to the cortex or descending projections to the spinal cord promote the changes in cortical activity and behavior that underlie the sleep–wake cycle and three states of waking, NREM (slow wave) sleep, and REM (paradoxical) sleep. Forming the basic units of these systems, glutamate and GABA cell groups are heterogeneous in discharge profiles and projections, such that different subgroups can promote cortical activation (wake/REM(PS)-active) versus cortical deactivation (NREM(SWS)-active) by ascending influences or behavioral arousal with muscle tone (wake-active) versus behavioral quiescence with muscle atonia (NREM/REM(PS)-active) by descending influences. These different groups are in turn regulated by neuromodulatory systems, including cortical activation (wake/REM(PS)-active acetylcholine neurons), behavioral arousal (wake-active noradrenaline, histamine, serotonin, and orexin neurons), and behavioral quiescence (NREM/REM(PS)-active MCH neurons). By different projections, chemical neurotransmitters and discharge profiles, distinct cell groups thus act and interact to promote cyclic oscillations in cortical activity and behavior forming the sleep-wake cycle and states.

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27

Tseng, Kuei-Yuan, and Marco Atzori. Monoaminergic Modulation of Cortical Excitability. Springer London, Limited, 2007.

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28

(Editor), Kuei-Yuan Tseng, and Marco Atzori (Editor), eds. Monoaminergic Modulation of Cortical Excitability. Springer, 2007.

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29

Tseng, Kuei-Yuan, and Marco Atzori. Monoaminergic Modulation of Cortical Excitability. Springer, 2010.

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30

The connection of brains theory. openlibrary, 2022.

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31

Duman, Ronald S. Neurotrophic Mechanisms of Depression. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0027.

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Early theories of depression and treatment response were centered on the monoamine neurotransmitters, but more recent work has focused on functional and structural synaptic plasticity and the role of neurotrophic factors, particularly brain derived neurotrophic factor (BDNF). Neurotrophic factors regulate all aspects of neuronal function, including adaptive plasticity, synapse formation, and neuronal survival. Chronic stress and depression cause reductions in levels of BDNF and other key factors, including vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF2), in cortical regions that contribute to atrophy and loss of neurons observed in depressed patients and rodent stress models. In contrast, these neurotrophic factors are upregulated by chronic administration of typical antidepressants and are required for antidepressant responses. Moreover, fast acting, highly efficacious antidepressant agents such as ketamine rapidly increase BDNF release and synapse formation, paving the way for a new generation of medications for the treatment of depression.

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32

Bleck, Thomas P. Pathophysiology and causes of seizures. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0231.

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Seizures result from imbalances between excitation and inhibition, and between neuronal synchrony and dyssynchrony. Current models implicate the cerebral cortex in the genesis of seizures, although thalamic mechanisms (particularly the thalamic reticular formation) are involved in the synchronization of cortical neurons. Often, the precipitants of a seizure in the critical care setting are pharmacological. Several mechanisms linked to critical illness can lead to seizures. Failure to remove glutamate and potassium from the extracellular space, functions performed predominantly by astrocytes, occurs in trauma, hypoxia, ischaemia, and hypoglycaemia. Loss of normal inhibition occurs during withdrawal from alcohol and other hypnosedative agents, or in the presence of GABA. Conditions such as cerebral trauma, haemorrhages, abscesses, and neoplasms all produce physical distortions of the adjacent neurons, astrocytes, and the extracellular space. Deposition of iron in the cortex from the breakdown of haemoglobin appears particularly epileptogenic. Although acute metabolic disturbances can commonly produce seizures in critically-ill patients, an underlying and potentially treatable structural lesion must always be considered and excluded.

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33

Clark, Kelsey L., Behrad Noudoost, Robert J. Schafer, and Tirin Moore. 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/9780199675111.013.010.

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Covert spatial attention prioritizes the processing of stimuli at a given peripheral location, away from the direction of gaze, and selectively enhances visual discrimination, speed of processing, contrast sensitivity, and spatial resolution at the attended location. While correlates of this type of attention, which are believed to underlie perceptual benefits, have been found in a variety of visual cortical areas, more recent observations suggest that these effects may originate from frontal and parietal areas. Evidence for a causal role in attention is especially robust for the Frontal Eye Field, an oculomotor area within the prefrontal cortex. FEF firing rates have been shown to reflect the location of voluntarily deployed covert attention in a variety of tasks, and these changes in firing rate precede those observed in extrastriate cortex. In addition, manipulation of FEF activity—whether via electrical microstimulation, pharmacologically, or operant conditioning—can produce attention-like effects on behaviour and can modulate neural signals within posterior visual areas. We review this evidence and discuss the role of the FEF in visual spatial attention.

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34

Daskalakis, Zafiris J., and Robert Chen. Evaluating the interaction between cortical inhibitory and excitatory circuits measured by TMS. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0012.

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Transcranial magnetic stimulation was first introduced in the late 1980s. Numerous studies have used TMS as an investigational tool to elucidate cortical physiology and to probe cognitive processes. This article introduces TMS paradigms and presents information gathered on cortical neuronal connectivity. TMS paradigms that demonstrate intracortical inhibition include short-interval cortical inhibition (SICI), cortical silence period (cSP) and long interval cortical inhibition (LICI). There are two types of cortical inhibitions from the stimulation of other brain areas, interhemispheric inhibition and cerebellum inhibition. The inhibition of the motor cortex can also be induced through the stimulation of peripheral nerves. This article talks about studies that describe interaction between inhibitory and facilitatory paradigms, the results of which are discussed in terms of cortical physiology and connectivity. The study of the interactions among cortical inhibitory and excitatory circuits may help to elucidate pathophysiology of neurological and psychiatric diseases.

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35

Anderson, James A. Loose Ends. Oxford University Press, 2018. http://dx.doi.org/10.1093/acprof:oso/9780199357789.003.0017.

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This chapter presents some ideas about Ersatz Brain Theory, which generalizes models presented in the book. It is based on three equal components: computation, cognition, and neuroscience. In the Ersatz Brain, the basic computing elements are locally interconnected groups of neurons, for example, cortical columns, and not single neurons. Columns are more powerful than neurons alone because of the potential for selectivity and reliability. A “network of networks” modular architecture is formed from interconnected groups. Response selection emerges from the stability properties of dynamical systems. Traveling waves and interference patterns also grow naturally out of dynamics and local connections. The resulting systems operate using similar rules at multiple spatial scales for different levels of integration.

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36

Genetic Control of Neuronal Migrations in Human Cortical Development (Advances in Anatomy, Embryology and Cell Biology). Springer, 2007.

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37

Velazquez, Jose Luis Perez, and Richard Wennberg. Coordinated Activity in the Brain. Springer, 2009.

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38

Rockland, Kathleen, and Javier DeFelipe, eds. Why Have Cortical Layers? What Is the Function of Layering? Do Neurons in Cortex Integrate Information Across Different Layers? Frontiers Media SA, 2018. http://dx.doi.org/10.3389/978-2-88945-660-4.

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39

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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40

Aziz, Qasim, and James K. Ruffle. The neurobiology of gut feelings. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198811930.003.0005.

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“It’s a gut feeling.” Indeed, how and why do we get “gut feelings?” After the brain, the gut is the second most innervated bodily organ, diffusely interconnected with gastrointestinal afferent neurons. Whilst sensory neurons from the gut ascend by means of the spinal cord and vagal nerve to subcortical and higher cortical areas of the brain, caudally descending motor efferents from brain to gut seek to modulate gastrointestinal function. Such is the construct of the “brain–gut axis,” a bi-directional body nexus permitting constant information transfer between both brain and gut so as to provide us with visceral interoception. This chapter reviews the neurobiology of gut feelings and discuss their role in both physical and mental health and disease.

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41

Saalmann, Yuri B., and Sabine Kastner. Neural Mechanisms of Spatial Attention in the Visual Thalamus. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.013.

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Neural mechanisms of selective attention route behaviourally relevant information through brain networks for detailed processing. These attention mechanisms are classically viewed as being solely implemented in the cortex, relegating the thalamus to a passive relay of sensory information. However, this passive view of the thalamus is being revised in light of recent studies supporting an important role for the thalamus in selective attention. Evidence suggests that the first-order thalamic nucleus, the lateral geniculate nucleus, regulates the visual information transmitted from the retina to visual cortex, while the higher-order thalamic nucleus, the pulvinar, regulates information transmission between visual cortical areas, according to attentional demands. This chapter discusses how modulation of thalamic responses, switching the response mode of thalamic neurons, and changes in neural synchrony across thalamo-cortical networks contribute to selective attention.

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42

Mauguière, François, and Luis Garcia-Larrea. Somatosensory and Pain Evoked Potentials. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0043.

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This chapter discusses the use of somatosensory evoked potentials (SEPs) and pain evoked potentials for diagnostic purposes. The generators of SEPs following upper limb stimulation have been identified through intracranial recordings, permitting the analysis of somatosensory disorders caused by neurological diseases. Laser activation of fibers involved in thermal and pain sensation has extended the applications of evoked potentials to neuropathic pain disorders. Knowledge of the effects of motor programming, paired stimulations, and simultaneous stimulation of adjacent somatic territories has broadened SEP use in movement disorders. The recording of high-frequency cortical oscillations evoked by peripheral nerve stimulation gives access to the functioning of SI area neuronal circuitry. SEPs complement electro-neuro-myography in patients with neuropathies and radiculopathies, spinal cord and hemispheric lesions, and coma. Neuroimaging has overtaken SEPs in detecting and localizing central nervous system lesions, but SEPs still permit assessment of somatosensory and pain disorders that remain unexplained by anatomical investigations.

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43

Wassermann, Eric M. Direct current brain polarization. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0007.

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The transcranial application of weak direct current (DC) to the brain is an effective neuromodulation technique that has had more than a century of experimental and therapeutic use. Focal DC brain polarization is now undergoing renewed interest, because of the wide acceptance of TMS as a research tool and candidate treatment for brain disorders. The effects of static electrical fields on cortical neurons in vivo have been known since the advent of intracellular recording. These effects are highly selective for neurons oriented longitudinally in the plane of the electric field. DC can enhance cognitive processes occurring in the treated area. The earliest clinical application of DC polarization was in the field of mood disorders. However, due to lack of temporal and spatial resolution, this technique does not appear particularly useful for exploring neurophysiological mechanisms.

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44

Montgomery, Erwin B. Discrete Neural Oscillators. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190259600.003.0017.

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The therapeutic mechanisms of action of DBS likely involve neural and neuronal oscillators. “Neuronal oscillators” describes periodic fluctuations of electrical potentials across the neuronal membrane, particularly in the soma, which is reflected in an action-potential-initiating segment. “Neural oscillators” describes closed loop (feedback) multi-neuronal polysynaptic circuits, on account of the propagations of action potentials through the circuit. Neural oscillators are the focus of this chapter. The features, properties and dyanmics introduced in Chapter 16 – Basic Oscillators are extended from continuous harmonic oscillators to discrete neural oscillators. While discrete oscillators received scant attention to date, systems of discrete oscillators have much richer set of dynamics that could provide better understanding of the pathophysiology and physiology of neural systems, such as the basal ganglia-thalamic-cortical system as well as greater insights into the therapeutic mechanisms of action underlying DBS.

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45

Buetefisch, Cathrin M., and Leonardo G. Cohen. Use-dependent changes in TMS measures. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0018.

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Adult brains maintain the ability to reorganize throughout life. Cortical reorganization or plasticity includes modification of synaptic efficacy as well as neuronal networks that carry behavioural implications. Transcranial magnetic stimulation (TMS) allows for the study of primary motor cortex reorganization in humans. Motor-evoked potential (MEP) amplitudes change in response to practice. This article gives information about the effect of practice on TMS measures such as motor-evoked potential amplitudes, motor maps, paired-pulse measures, and behavioural measures. These changes may be accompanied by down-regulation of activity in nearby body part representations within the same hemisphere and in homonymous regions of the opposite hemisphere, mediated by interhemispheric interactions. There is evidence pointing towards the influence of practice on a distributed network of cortical representations within regions of cerebral hemispheres. This has lead to the formulation of intervention strategies to enhance the training effects by cortical or somatosensory stimulation in health and disease.

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46

Shin, Damian Seung-Ho. Examining gap junctions, NMDA and AMPA receptors for evidence of channel arrest in cortical neurons of the anoxia-tolerant turtle, Chrysemys picta bellii. 2005.

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47

Pinna, Baingio. On the Pinna Illusion. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199794607.003.0074.

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The Pinna illusion is the first case of visual illusion showing a rotating motion phenomenon. Squares, arranged in two concentric rings, show a strong counter-rotation effect. The inner ring of the squares appears to rotate counterclockwise and the outer ring clockwise when the observer’s head is slowly moved toward the figure while the gaze is kept fixed in the center of the stimulus pattern. The direction of rotation is reversed when the observer’s head moves away from the stimulus. The speed of the illusory rotation is proportional to the one of the motion imparted by the observer. While the way each individual check receives a local illusory motion signal can be explained by the response of direction-selective neurons at the earliest cortical stage of visual processing, the whole illusory rotational motion can be thought to be sensed by the higher cortical area, which collates all the signals provided by the local motion checks.

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48

Kotagal, Vikas, and Praveen Dayalu. Parkinson Syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0005.

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Progressive supranuclear palsy (PSP) is a neurodegenerative condition characterized by axial motor features, oculomotor abnormalities, and cognitive dysfunction. PSP is characterized by progressive tau deposition with neuronal loss in cortical and subcortical regions. The underlying etiology of PSP may reflect complex gene-environment interactions, though genetic heterogeneity in the microtubule-associated protein tau (MAPT) gene can confer increased risk. Clinical care of patients with PSP focuses on minimizing motor and non-motor morbidity using available symptomatic therapies.

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49

Beninger, Richard J. Life's rewards. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.001.0001.

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Life’s Rewards: Linking Dopamine, Incentive Learning, Schizophrenia, and the Mind explains how increased brain dopamine produces reward-related incentive learning, the acquisition by neutral stimuli of increased ability to elicit approach and other responses. Dopamine decreases may produce inverse incentive learning, the loss by stimuli of the ability to elicit approach and other responses. Incentive learning is gradually lost when dopamine receptors are blocked. The brain has multiple memory systems defined as “declarative” and “non-declarative;” incentive learning produces one form of non-declarative memory. People with schizophrenia have hyperdopaminergia, possibly producing excessive incentive learning. Delusions may rely on declarative memory to interpret the world as it appears with excessive incentive learning. Parkinson’s disease, associated with dopamine loss, may involve a loss of incentive learning and increased inverse incentive learning. Drugs of abuse activate dopaminergic neurotransmission, leading to incentive learning about drug-associated stimuli. After withdrawal symptoms have been alleviated by detoxification treatment, drug-associated conditioned incentive stimuli will retain their ability to elicit responses until they are repeatedly experienced in the absence of primary drug rewards. Incentive learning may involve the action of dopamine at dendritic spines of striatal medium spiny neurons that have recently had glutamatergic input from assemblies of cortical neurons activated by environmental and proprioceptive stimuli. Glutamate initiates a wave of phosphorylation normally followed by a wave of phosphatase activity. If dopaminergic neurons fire, stimulation of D1 receptors prolongs the wave of phosphorylation, allowing glutamate synaptic strengthening. Activity in dopaminergic neurons in humans appears to affect mental experience.

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50

Ziemann, Ulf. Pharmacology of TMS measures. Edited by Charles M. Epstein, Eric M. Wassermann, and Ulf Ziemann. Oxford University Press, 2012. http://dx.doi.org/10.1093/oxfordhb/9780198568926.013.0013.

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This article discusses various aspects of the pharmacology of transcranial magnetic stimulator (TMS) measures. TMS measures reflect axonal, or excitatory or inhibitory synaptic excitability in distinct interneuron circuits. TMS measures can be employed to study the effects of a drug with unknown or multiple modes of action, and hence to determine its main mode of action at the systems level of the motor cortex. TMS experiments can also study acute drug effects that may be different from chronic drug effects. TMS or repetitive TMS may induce changes in endogenous neurotransmitter or neuromodulator systems. This allows for the study of neurotransmission along defined neuronal projections in health and disease. This article describes pharmacological experiments that have characterized the physiology of TMS measures of motor cortical excitability. Pharmacological challenging of TMS measures has opened a broad window into human cortical physiology.

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Books on the topic 'Neuroni corticali'

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