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1
Thomas, Schiex, ed. Intelligence artificielle et informatique théorique. Toulouse: Cépaduès-éd., 1994.
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2
Baldi, Elisabetta, and Corrado Bucherelli. Neuroscience. Florence: Firenze University Press, 2017. http://dx.doi.org/10.36253/978-88-6453-638-5.
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This bibliographic material is patrimony of our Laboratory of the Behavior Physiology. This research unit originated in 1972 by will of Aldo Giachetti (until 1990) and with the beginning of the activity of Corrado Bucherelli. In the early 1980s, with Carlo Ambrogi Lorenzini (until 2004), the cataloging became more capillary and systematic, to continue to this day. All the researchers who worked in our laboratory contributed to this collection (Giovanna Tassoni 1986-2000, Benedetto Sacchetti 1996-2002 and Elisabetta Baldi from 1991). The study of learning, memory and behavior requires to follow a broad spectrum of neuroscience topics, ranging from neuronal biochemistry to neuropsychology. The Authors’ idea of publishing this collection comes from believing that a such website, though not exhaustive, might be a useful and targeted tool for the selection of bibliographic material in the field of behavioral neuroscience. The bibliographic references present at the publication (29500), accompanied by a brief comment highlighting the contents, are organized in relation to the topics (represented by the 99 themes) constituting the publication itself. The intersection of several references will point out the topics that represent them simultaneously. Concerning neurotransmitters and neuromodulators, references to agonists, antagonists or molecules interfering with the activity of these synapses have been inserted in the pages of the implicated neurotransmitter (e.g. acetylcholine). The pages including topics that could have been dealt with separately (e.g. active and passive avoidance) are introduced by a short explanatory note. The comment of each publication highlights the animal species used. Each comment is intended to indicate the content rather than the experimental results of paper. This choice comes from wanting to provide the reader with a more objective and less speculative comment.
3
Montgomery, Erwin B. Controlling the Flow of Electrical Charges. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190259600.003.0004.
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In depolarization to effect neuronal activations,, electrical charges are delivered to the neuron to affect the electrical potential across the neuronal membrane to subsequently affect voltage-gated ionic conductance channels. The orientation of the field of electrical charges to the neuronal membrane is critical. Electrical charges flow from the negative contact to the positive contact. The negative electrostatic charge “pushes” negative charges onto the outer surface of the neuron, which results in depolarization of the neuronal membrane. Neurons near the positive contact will not have negative electrical charges deposited on the outer surface, will not be depolarized, and thus, are not activated. Likewise, neurons whose membranes are oriented parallel to the lines of electrical forces that move electrical charges will not receive the electrical charges and, consequently, will not be activated. The electronics of the DBS systems are designed to control the electrostatic forces so as to control the activations of the nervous system to generate benefit and avoid adverse effects.
4
Soffietti, Riccardo, Hugues Duffau, Glenn Bauman, and David Walker. Neuronal and mixed neuronal–glial tumours. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0008.
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Neuronal and mixed neuronal-glial tumours are rare tumours of the central nervous system that occur more commonly in children. Despite a generally benign course, most tumours cause medically intractable seizures, and have been denominated as ‘long-term epilepsy-associated tumours’. The World Health Organization classification distinguishes nine histological variants: dysplastic gangliocytoma of the cerebellum/Lhermitte–Duclos disease, desmoplastic infantile astrocytoma and ganglioglioma, dysembryoplastic neuroepithelial tumour, gangliocytoma and ganglioglioma, central neurocytoma and extraventricular neurocytoma, cerebellar liponeurocytoma, papillary glioneuronal tumour, rosette-forming glioneuronal tumour of the fourth ventricle, and spinal paraganglioma. Early surgery with complete resection may significantly improve the likelihood of postoperative epilepsy freedom. Conformal radiotherapy can be considered in case of patients with incompletely resected symptomatic tumours, atypical or high-grade tumours, or in the case of multiple recurrences despite resections. The role of chemotherapy in these lesions remains poorly defined, while targeted therapies are now available to impact some molecular alterations.
5
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.
6
Nieder, Andreas. Neuronal Correlates of Non-verbal Numerical Competence in Primates. Edited by Roi Cohen Kadosh and Ann Dowker. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199642342.013.027.
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Non-verbal numerical competence, such as the estimation of set size, is rooted in biological primitives that can also be explored in animals. Over the past years, the anatomical substrates and neuronal mechanisms of numerical cognition in primates have been unravelled down to the level of single neurons. Studies with behaviourally-trained monkeys have identified a parietofrontal network of individual neurons selectively tuned to the number of items (cardinal aspect) or the rank of items in a sequence (ordinal aspect). The properties of these neurons’ numerosity tuning curves can explain fundamental psychophysical phenomena, such as the numerical distance and size effect. Functionally overlapping groups of parietal neurons represent not only numerable-discrete quantity (numerosity), but also innumerable-continuous quantity (extent) and relations between quantities (proportions), supporting the idea of a generalized magnitude system in the brain. Moreover, many neurons in the prefrontal cortex establish semantic associations between signs and abstract numerical categories, a neuronal precursor mechanisms that may ultimately give rise to symbolic number processing in humans. These studies establish putative homologies between the monkey and human brain, and demonstrate the suitability of non-human primates as model system to explore the neurobiological roots of the brain’s non-verbal quantification system, which may constitute the phylogenetic and ontogenetic foundation of all further, more elaborate numerical skills in humans.
7
DeFelipe, Javier. Cajal's Neuronal Forest. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190842833.001.0001.
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Cajal’s Neuronal Forest: Science and Art continues the tradition set forth in the 2009 publication Cajal’s Butterflies of the Soul: Science and Art. This new compilation contains a vastly large collection of beautiful figures produced throughout the nineteenth century and the beginning of the twentieth century. These images continue to represent and illustrate characteristic examples of the early days of research in neuroscience. Most scientific figures presented by the neuroanatomists of the time were their own drawings; microphotography was not yet a well-developed technique. Therefore, a successful neuroanatomist required a combination of artistic talent and an ability to interpret microscopic images effectively. The problem was that these illustrations were not necessarily free of technical errors and they may have been subject to the scientists’ own interpretations. Indeed, in some cases, these drawings were considered to be basically artistic interpretations rather than accurate copies of the histological preparations. Furthermore, there are many examples showing that even using the same microscopes and the same techniques, scientists “see” differently through the microscope. As a result, this period of scientific “art” and skepticism represents a fascinating page in the history of neuroscience as it provided the basis of our current understanding of the anatomy of the nervous system.
8
Caillaud, Catherine, and Frédéric Sedel. Neuronal Ceroid Lipofuscinoses. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0059.
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Neuronal ceroid lipofuscinoses (NCLs) are inherited neurodegenerative disorders beginning mainly in childhood, rarely in adults. They are characterized by the accumulation of autofluorescent lipopigments in brain, especially in neurons. Their clinical heterogeneity is now explained by the huge number of genes (from CLN1 to CLN14) involved in their pathogenesis. Their diagnosis is possible using enzymatic tests and/or direct sequencing of the corresponding genes. Different therapeutic approaches are in development for these diseases such as enzyme replacement therapy or gene transfer.
9
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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Coleman, William L., and R. Michael Burger. Extracellular Single-Unit Recording and Neuropharmacological Methods. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199939800.003.0003.
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Small biogenic changes in voltage such as action potentials in neurons can be monitored using extracellular single unit recording techniques. This technique allows for investigation of neuronal electrical activity in a manner that is not disruptive to the cell membrane, and individual neurons can be recorded from for extended periods of time. This chapter discusses the basic requirements for an extracellular recording setup, including different types of electrodes, apparatus for controlling electrode position and placement, recording equipment, signal output, data analysis, and the histological confirmation of recording sites usually required for in vivo recordings. A more advanced extracellular recording technique using piggy-back style multibarrel electrodes that allows for localized pharmacological manipulation of neuronal properties is described in detail. Strategies for successful signal isolation, troubleshooting advice such as noise reduction, and suggestions for general laboratory equipment are also discussed.
11
Uffman, Joshua C. Neuronal Ceroid Lipofuscinoses (Batten Disease). Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0042.
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Neuronal ceroid lipofuscinoses (NCL) are a group of autosomal recessive genetic disorders which represent the most common form of childhood neurodegenerative disease. Classically the disease was described according to the age of diagnosis resulting in four common phenotypes: (i) infantile or Santavuori-Haltia, (ii) late infantile or Jansky-Bielschowsky, (iii) juvenile or Spielmeyer-Vogt, and (iv) adult or Kufs. With advances in genetic mutational analysis techniques and improved understanding of NCL disease as a whole, disease classification now focuses on which of the known genetic defects is responsible for the disease. Regardless of genetic defect or age of onset, patients typically present with language delay, seizures, blindness, and ataxia. The term “Batten disease” is used to refer to the group as a whole in addition to specifically referring to the juvenile form. Anesthetic implications focus on disease symptoms at presentation, with special attention to maintaining normorthermia and the possibility of bradycardia.
12
Thakore, Nimish, and Erik P. Pioro. Types of Motor Neuron Diseases. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0022.
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Disorders of lower motor neurons (LMNs, or anterior horn cells) and upper motor neurons (UMNs), jointly termed motor neuron disorders (MNDs), are diverse and numerous. The prototypical MND, namely amyotrophic lateral sclerosis (ALS), a relentlessly progressive lethal disorder of adults, is the subject of another section and will not be discussed further here. Other MNDs include spinal muscular atrophy (SMA), of which there are four types: Kennedy’s disease, Brown-Violetto-Van Laere, and Fazio-Londe syndromes, lower motor neuron disorders as part of neurodegenerations and secondary motor neuron disease as part of malignancy, radiation and infection.
13
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.
14
Bloom, Molly. ¡Está Vivo!: De Las Neuronas y Los Narvales a Los Hongos Que Nos Rodean. Editorial Oceano de Mexico, 2022.
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15
Soileau, Michael J., and Kelvin L. Chou. Parkinson Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0002.
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Parkinson disease is a neurodegenerative disorder characterized clinically by tremor, rigidity, bradykinesia, and postural instability and pathologically by loss of nigrostriatal neurons and deposition of alpha-synuclein in neuronal cell bodies and neuritis. Non-motor symptoms such as psychiatric disorders, cognitive abnormalities, sleep dysfunction, autonomic dysfunction, and sensory manifestations are also common. This chapter gives a broad overview of this disorder. Sections cover pathophysiology, genetics, clinical manifestations, and disease course. The chapter also briefly discusses how to make the diagnosis, and alternative conditions that should be considered.
16
Magnussen, Claire, and Alfredo Ribeiro-da-Silva. Plasticity. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0043.
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This chapter discusses the landmark paper ‘Neuronal plasticity: increasing the gain in pain’, published by Woolf and Salter in 2000. Excellent review articles not only give a concise overview of a topic but also provide a framework for future research. In 2000, Clifford Woolf and Michael Salter joined forces to write one of the most highly cited review articles in the field of pain research and thus provided a conceptual framework for the plastic changes that occur in nociceptive neurons in response to chronic pain. With over 2,700 citations, this review is one of those rare articles that is still appreciated by pain researchers across domains.
17
Morse, Stephen J. The Neuroscientific Non-Challenge to Meaning, Morals, and Purpose. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190460723.003.0018.
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Stephen J. Morse argues that neuroscience raises no new challenges for the existence, source, and content of meaning, morals, and purpose in human life, nor for the robust conceptions of agency and autonomy underpinning law and responsibility. Proponents of revolutionizing the law and legal system make two arguments. The first appeals to determinism and the person as a “victim of neuronal circumstances” (VNC) or “just a pack of neurons” (PON). The second defend “hard incompatibilism. ” Morse reviews the law’s psychology, concept of personhood, and criteria for criminal responsibility, arguing that neither determinism nor VNC/PON are new to neuroscience and neither justifies revolutionary abandonment of moral and legal concepts and practices evolved over centuries in both common law and civil law countries. He argues that, although the metaphysical premises for responsibility or jettisoning it cannot be decisively resolved, the hard incompatibilist vision is not normatively desirable even if achievable.
18
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.
19
Shaw, Pamela. The motor neurone disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0524.
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The motor neurone diseases are a group of disorders in which there is selective loss of function of upper and/or lower motor neurones in the motor cortex, brainstem, and spinal cord resulting in impairment in the nervous system control of voluntary movement. The term ‘motor neurone disease’, often abbreviated to ‘MND’, is used differently in different countries. In the United Kingdom it is used as an umbrella term to cover the related group of neurodegenerative disorders including amyotrophic lateral sclerosis, the commonest variant, as well as progressive muscular atrophy, primary lateral sclerosis, and progressive bulbar palsy. However, in many other countries amyotrophic lateral sclerosis, referred to as ALS, has been adopted as the umbrella term for this group of clinical variants of motor system degeneration. There is a tendency now internationally to use the ALS/MND abbreviation to cover this group of conditions. Careful diagnosis within the motor neurone diseases is essential for advising about prognosis, potential genetic implications, and for identifying those with acquired lower motor neurone syndromes who may benefit for the administration of immunomodulatory therapy.
20
Dickenson, Tony. A new theory of pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0007.
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Of all the seminal papers on pain, the one described in this chapter must be one of the most influential. It has been cited over 11,000 times. This paper proposed the theory that the transmission of pain from peripheral fibres through the spinal cord to the brain was not a passive fixed process but was subject to modulation and alteration. It also suggested that there was interplay between different afferent fibres, spinal excitatory neurons, and inhibitory spinal neuron and that the brain could exert influence on the spinal cord. Most of modern pain science and clinical management is based on this theory, which is now clearly backed up by facts.
21
McLaren, Anya T. Increased expression of hypoxia inducible factor-1alpha (HIF-1alpha) and neuronal nitric oxide synthase (nNOS) in the cerebral cortex of anemic rats. 2006.
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22
Kilintari, Marina, and Andrew C. Papanicolaou. Imaging the Networks of Voluntary Actions. Edited by Andrew C. Papanicolaou. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199764228.013.22.
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The concept of voluntary actions is inextricably related to the concept of the will. Accordingly, in the first section of this chapter, the authors examine briefly the neuroimaging evidence for a neuronal mechanism of human will and decision-making and conclude that what evidence is brought to bear on the issue may not be relevant to it after all. In the second section, a review of the known mechanism for self-initiated as well as externally mediated voluntary actions is presented against which the contributions of functional neuroimaging to improving our knowledge for simple and complex actions can be judged. In the final section differences in the neuronal networks mediating decisions as to when to act and what action to select are explored.
23
Beninger, Richard J. Schizophrenia, Parkinson’s disease, and attention deficit hyperactivity disorder. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0009.
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Schizophrenia, Parkinson’s disease, and attention deficit hyperactivity disorder (ADHD) discusses how hyperactive dopaminergic neurotransmission appears to underlie schizophrenia’s positive symptoms, loss of dopaminergic neurons in adulthood leads to Parkinson’s disease, and dopamine neuron hypofunction in childhood and adolescence may underlie ADHD. Positive schizophrenia symptoms may arise from excessive incentive learning that is gradually lost with antipsychotic treatment. Declarative learning and memory may contribute to delusions based on excessive incentive learning. Loss of responsiveness to environmental stimuli in Parkinson’s may result from a decrease of their conditioned incentive value and inverse incentive learning. Conditioned incentive stimuli not encountered while in a state of decreased dopaminergic neurotransmission may retain their incentive value, producing apparent kinesia paradoxa. Dopamine hypofunction in juveniles does not lead to hypokinesia but may result in loss of incentive learning that focuses attention. Pro-dopaminergic drugs have a calming effect in ADHD, presumably because they reinstate normal incentive learning.
24
van der Burg, Jorien M. M., N. Ahmad Aziz, and Maria Björkqvist. Peripheral Pathology. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199929146.003.0014.
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Clinicians and researchers have previously focused on the neurologic and psychiatric aspects of Huntington’s disease (HD). However, it is becoming evident that many neurodegenerative disorders are also complicated by pathology in tissues outside the brain. Although many clinical features of HD can be ascribed to neuronal loss and dysfunction, there is accumulating evidence indicating a role for the pathology of non-neuronal tissues in the disease process. Mutant huntingtin is expressed throughout the body and may induce pathology in parallel in both the brain and other organs. Insights into peripheral pathology in HD have the potential of improving knowledge of key pathogenic mechanisms. This chapter describes peripheral manifestations of HD, including weight loss, muscle wasting, and cardiac dysfunction, and discusses how these might constitute targets for drug treatment as well as offering disease modeling systems and potential sources of biomarkers.
25
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.
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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
26
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.
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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
27
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.
Full textAbstract:
Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
28
Kalitzin, Stiliyan, and Fernando Lopes da Silva. EEG-Based Anticipation and Control of Seizures. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0023.
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Early seizure-prediction paradigms were based on detecting electroencephalographic (EEG) features, but recent approaches are based on dynamic systems theory. Methods that attempted to detect predictive features during the preictal period proved difficult to validate in practice. Brain systems can display bistability (both normal and epileptic states can coexist), and the transitions between states may be initiated by external or internal dynamic factors. In the former case prediction is impossible, but in the latter case prediction is conceivable, leading to the hypothesis that as seizure onset approaches, the excitability of the underlying neuronal networks tends to increase. This assumption is being explored using not only the ongoing EEG but also active probes, applying appropriate stimuli to brain areas to estimate the excitability of the neuronal populations. Experimental results support this assumption, suggesting that it may be possible to develop paradigms to estimate the risk of an impending transition to an epileptic state.
29
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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Chappell, Michael, Bradley MacIntosh, and Thomas Okell. Using ASL to Measure Perfusion Changes in an Individual: Task-Based ASL and Beyond. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198793816.003.0007.
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Arterial spin labeling (ASL) MRI measurements of perfusion provide a flexible and unique way to study the brain’s physiology and function. They enable experimental designs in neuroimaging that can complement widely used blood oxygen level dependent functional MRI (BOLD fMRI) experiments, or even enable experiments not possible with BOLD fMRI. This chapter explores ways in which ASL can be used to detect changes in perfusion in an individual, including those that involve stimulation of neuronal activity or pharmacological intervention.
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Gallagher, Shaun. Action and the Problem of Free Will. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198794325.003.0007.
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This chapter examines the concept of free will as it is discussed in philosophy and neuroscience. It reviews reflective and perceptual theories of agency and argues against neuro-centric conclusions about the illusory nature of free will. Experiments conducted by Benjamin Libet suggest that neural activations prior to conscious awareness predict specific actions. This has been taken as evidence that challenges the traditional notion of free will. Libet’s experiments, arguably, are about motor control processes on an elementary timescale and say nothing about freely willed intentional actions embedded in personal and social contexts that involve longer-term, narrative timescales. One implication of this interpretation is that enactivism is not a form of simple behaviorism. Agency is not a thing reducible to elementary neuronal processes; nor is it an idea or a pure consciousness. It rather involves a structure of complex relations.
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Clark, Caroline, Jeffrey Cole, Christine Winter, and Geoffrey Grammer. Transcranial Magnetic Stimulation Treatment of Posttraumatic Stress Disorder. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190205959.003.0005.
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Symptoms of post-traumatic stress disorder (PTSD) often fail to resolve with psychotherapy, pharmacotherapy, or integrative medicine treatments. Given these limitations, there is a continued push to discover treatment methods utilizing novel mechanisms of action. Transcranial magnetic stimulation (TMS) offers a non-invasive and safe method of brain stimulation that modulates neuronal activity in a focal area to achieve excitation or inhibition, and may have utility for patients suffering from PTSD, although, to date, evidence of efficacy is limited. The TMS treatment can be varied to suit the needs of the patient by altering the selection of the specific treatment parameters, such as pulse frequency or stimulation intensity. The weight of evidence to date supports treatment of either the right dorsolateral prefrontal cortex or the medical prefrontal cortex. Coupling treatment with script based exposure therapies may also assist with potentiation of the extinction response. Ultimately, stimulation parameters may be related to secondary downstream effects, and thus current targets may indirectly reverse the underlying neuronal pathophysiology. Given that PTSD is a complex illness with a poorly understood pathophysiology, it often exists with other psychiatric comorbidities or TBI. As such, TMS could be an effective part of a comprehensive treatment program.
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Katirji, Bashar. Case 19. Edited by Bashar Katirji. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603434.003.0023.
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Amyotrophic lateral sclerosis is a fatal neurological disorder, classically presenting with signs of upper motor neuron and lower motor neuron degeneration. Several motor neuron disease variants with purely upper or lower motor neuron degeneration exist. These includes primary lateral sclerosis, progressive muscular atrophy and progressive bulbar palsy. The diagnostic criteria, including El-Escorial criteria and its most recent Awaji revision, are not used in clinical practice and for research purposes. This case highlights the clinical features and electrodiagnostic characteristics of amyotrophic lateral sclerosis. The findings on nerve conduction studies and needle electromyography are emphasized in detail. The role of electrodiagnostic studies in the diagnosis of amyotrophic lateral sclerosis is to establish evidence of lower motor neuron degeneration, confirm its diffuse nature, and exclude treatable causes (such as multifocal motor neuropathy and mimickers of motor neuron disease such as chronic myopathies).
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Lei, Peng, Scott Ayton, and Ashley I. Bush. Metal-Protein Attenuating Compounds in Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0015.
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Neurodegenerative disorders including Alzheimer’s (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS) are progressive diseases of the aging population with currently few therapeutic options. While aggregation and deposition of disease-specific proteins link the pathologies of these diseases, targeting these aggregating proteins with therapeutics has not yet been successful in clinical trial. This chapter profiles metals (copper, zinc, and iron) as alternative drug targets for neurodegeneration. Complex changes to metals occur in these neurodegenerative diseases. Accumulating evidences have demonstrated that perturbations to metal homeostasis contribute to the progression of neuronal dysfunction and death. Importantly, several phase II trials have shown that correcting metal dyshomeostasis improves clinical outcomes; the chapter argues that it is now time to explore the therapeutic utility of metal-based drugs in larger, phase III trials.
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Goodman, Wayne K., and Mark S. George. Neuromodulation and Psychiatric Disorders. 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/9780190681425.003.0010.
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An increasing number of approaches permit psychiatrists to directly stimulate the brain. Such therapies are sometimes referred to as neuromodulation, as psychiatrists can either excite or inhibit neuronal firing in the brain. This chapter reviews two such technologies—transcranial magnetic stimulation (TMS) and deep brain stimulation (DBS). Both techniques have FDA approval and are moving into mainstream therapeutic use. Daily prefrontal TMS for 4–6 weeks is FDA approved for treating depression, with minimal side effects. It is now accepted in most treatment algorithms as an approach for patients who have not responded to medications or talking therapy. DBS has virtually replaced ablative neurosurgery for use in medication-refractory movement disorders such as Parkinson’s Disease (PD), where it has the advantages of being reversible (explantable) and adjustable. DBS is now being studied in severe psychiatric conditions, such as intractable obsessive-compulsive disorder (OCD) and treatment resistant depression (TRD).
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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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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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Tononi, Giulio, and Chiara Cirelli. The Neurobiology of Sleep. 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/9780190681425.003.0011.
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Sleep is required for health and well-being, and consumes roughly one-third of a human’s lifetime, yet its functions remain incompletely understood. This chapter provides an overview of so-called sleep architecture—the stages and cycles that characterize sleep, including rapid eye movement (REM) and non-REM periods. Also discussed are the numerous regions of brain and neurotransmitters that control the induction of sleep, the transitions between REM and non-REM sleep cycles, and wakefulness. Key brain systems include GABAergic neurons in the pre-optic area, the neuropeptide orexin in lateral hypothalamic neurons, histaminergic neurons in the hypothalamus, monoaminergic (norepinephrine and serotonin) and acetylcholinergic nuclei in the brainstem, and the brain’s adenosine system, all of which work in integrated circuits to control sleep and wakefulness. Overlaid on sleep-wake cycles are circadian rhythms, and the crucial role played by the suprachiasmatic nucleus in entraining such rhythms to environmental light.
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Bauer, Jan, and Christian G. Bien. Rasmussen Encephalitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0096.
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Rasmussen encephalitis (RE) is a rare epileptic disorder that is characterized by the presence of unihemispheric seizures coinciding with inflammation. The disease mostly presents in children. Clinically, patients often reach a residual stage with drug resistant seizures and severe neurological deficits. Pathologically, at this stage, the brain shows variable neuronal loss. The etiology is unknown but the infiltration of large numbers of CD8 positive T lymphocytes suggests that this is an autoimmune disease. Treatment consists of anti-inflammatory therapy (IVIG or tacrolimus), which, however, does not reduce the drug-resistant seizures. Therefore, hemisperectomy is the most effective treatment of RE.
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DeFelipe, Javier. The Golden Era for Artistic Creativity in Neuroscience. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190842833.003.0003.
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Section B focuses on the artistic skills and emotions of Cajal and other important pioneers in neuroscience, using their own words to describe the artistic emotions they experienced when visualizing the neural elements. This section also deals with the verification in recent years of many of the descriptions and illustrations of the early neuroanatomists, particularly those of Cajal. The last part of this section describes how the neuronal forests have served as an unlimited source of artistic and poetic inspiration to many scientists, not only in the early days of the research of the brain, but also in modern times.
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Gallagher, Shaun, Ben Morgan, and Naomi Rokotnitz. Relational Authenticity. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190460723.003.0008.
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In Chapter 8, the authors explore the notion of relational authenticity, arguing that to understand existential authenticity we must not return to the individuality celebrated by classical existentialism nor look for a reductionist explanation in terms of neuronal patterns or mental representations that would simply opt for a more severe methodological individualism and a conception of authenticity confined to proper brain processes. Rather, they propose, we should look for a fuller picture of authenticity in what they call the “4Es”—the embodied, embedded, enactive, and extended conception of mind. They argue that one requires the 4Es to maintain the 4Ms—mind, meaning, morals, and modality—in the face of reductionistic tendencies in neurophilosophy. The 4E approach, they contend, gives due consideration to the importance of the brain, taken as part of the brain-body-environment system, incorporating neuroscience and integrating phenomenological-existentialist conceptions that emphasize embodiment and the social environment.
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Massimini, Marcello, and Giulio Tononi. Mysteries in the Cranium. Translated by Frances Anderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198728443.003.0004.
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This chapter exposes a series of fundamental paradoxes about the relationships between consciousness and the brain—why does the cortex support consciousness, but not the cerebellum, which has four times more neurons? Why does consciousness vanish during deep sleep, even though the neurons remain active? How can the vivid experience of a dream be generated without interactions with the environment? These facts are in front of our eyes, they are tangible both clinically and experimentally, and prompt an interesting consideration. Maybe, what we need at this stage is not another experiment, but rather a principle; a starting point to combine the available, before we can formulate novel predictions.
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Massimini, Marcello, and Giulio Tononi. Reappraising the Stuff in Our Head. Translated by Frances Anderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198728443.003.0006.
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This chapter addresses the questions posed in Chapter 4. Using the general principle introduced in Chapter 5 as a guide, it reappraises different anatomical structures within the skull. Once analyzed under the perspective of IIT, the paradoxes posed by cerebellum, the basal ganglia, and by other large neuronal aggregates that seem irrelevant for consciousness, are less disconcerting; their architecture is not suited for integrating information, whereas the thalamocortical system seems to contain a core of high Φ. The chapter ends by suggesting that the time scale at which conscious experience flows (hundreds of milliseconds) may be related to the time it takes for the brain to integrate information.
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Seeck, Margitta, L. Spinelli, Jean Gotman, and Fernando H. Lopes da Silva. Combination of Brain Functional Imaging Techniques. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0046.
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Several tools are available to map brain electrical activity. Clinical applications focus on epileptic activity, although electric source imaging (ESI) and electroencephalography-coupled functional magnetic resonance imaging (EEG–fMRI) are also used to investigate non-epileptic processes in healthy subjects. While positron-emission tomography (PET) reflects glucose metabolism, strongly linked with synaptic activity, and single-photon-emission computed tomography (SPECT) reflects blood flow, fMRI (BOLD) signals have a hemodynamic component that is a surrogate signal of neuronal (synaptic) activity. The exact interpretation of BOLD signals is not completely understood; even in unifocal epilepsy, more than one region of positive or negative BOLD is often observed. Co-registration of medical images is essential to answer clinical questions, particularly for presurgical epilepsy evaluations. Multimodal imaging can yield information about epileptic foci and underlying networks. Co-registering MRI, PET, SPECT, fMRI, and ESI (or magnetic source imaging) provides information to estimate the epileptogenic zone and can help optimize surgical results.
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Krauzlis, Richard J. Attentional Functions of the Superior Colliculus. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.014.
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The superior colliculus (SC) plays an important role in both overt and covert attention. In primates, the SC is well known to be a central component of the motor pathways that orient the eyes and head to important objects in the environment. Accordingly, neurons in the SC show enhanced responses that will be the target of orienting movements, compared to stimuli that will be ignored. Single-neuron recordings in the SC have revealed a variety of attention-related effects, including changes in activity related to bottom-up and top-down attention, attention capture, and inhibition of return. These findings support the view of the SC as a priority map that represents the location of important objects in the visual environment. Manipulation of SC activity by electrical microstimulation and chemical inactivation shows that the SC is not simply a recipient of attention-related effects, but plays a causal role in these processes. In particular, activity in the SC plays a major role in the selection of targets for saccades, and also for pursuit eye movements and movements of the hand. Moreover, activity in the SC is important not only for the control of overt attention, but also plays a crucial role in covert attention—the processing of visual signals for perceptual judgements even in the absence of orienting movements. The mechanisms mediating the role of the SC in the control of covert attention are not yet known, but current models emphasize interactions between the SC and areas of the cerebral cortex.
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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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Papanicolaou, Andrew C., Nicole Shay, and Christen M. Holder. Imaging the Networks of Encoding, Consolidation, and Retrieval. Edited by Andrew C. Papanicolaou. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199764228.013.21.
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In this chapter, the authors examine the contributions of the functional neuroimaging literature to the specification of the neuronal networks of the mnemonic operations of encoding, consolidation, and retrieval. Although the most basic expectation regarding the involvement of parts of the medial temporal lobes, such as the hippocampus, in these operations was not consistently supported by the results of the neuroimaging studies reviewed, other expectations, such as the material-specific lateralization of activation were adequately supported. The several reasons that account for the limited contributions of neuroimaging to the neurophysiology of memory thus far, ranging from constraints imposed by the nature of the mnemonic operations (e.g., the fact that encoding and retrieval occur in tandem) to practical ones (e.g., difficulties in studying spontaneous retrieval), are outlined.
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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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Bates, David. Cauda equina lesions, radiculopathies, and sphincter disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0678.
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Pathological processes involving the spinal roots and cauda equina present with symptoms of lower motor neurone and first order sensory neurone damage. Pain is a common, though not inevitable, symptom. Pathological processes may be acute, as with a prolapsed intervertebral disc or chronic and extend over many years, as with spondylotic bony changes or structural diseases such as spondylolisthesis. The cauda equina carries innervation to the bladder, rectum, corpus cavernosum, and seminal vesicles and damage commonly presents with sphincter disturbance and impotence. In general the nerve roots throughout the spine and cauda equina are more resistant to injury and pathological processes than the spinal cord; rapid diagnosis and surgical intervention where indicated, may improve outcome considerably.
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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.