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Books on the topic 'Primary neuron'

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Published: 9 March 2023
Last updated: 10 March 2023

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1

Zenker, Wolfgang, and Winfried L. Neuhuber, eds. The Primary Afferent Neuron. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0579-8.

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2

1925-, Zenker W., and Neuhuber Winfried L, eds. The Primary afferent neuron: A survey of recent morpho-functional aspects. New York: Plenum Press, 1990.

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3

T, Thomas D. G., ed. Neuro-oncology: Primary malignant brain tumors. Baltimore: Johns Hopkins University Press, 1990.

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4

T, Thomas David G., ed. Neuro-oncology: Primary malignant brain tumours. London: Edward Arnold, 1990.

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5

Dabdoub, Alain, Bernd Fritzsch, Arthur N. Popper, and Richard R. Fay, eds. The Primary Auditory Neurons of the Mammalian Cochlea. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3031-9.

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6

Complex Encoding of Olfactory Information by Primary Sensory Neurons. [New York, N.Y.?]: [publisher not identified], 2020.

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7

A, Twijnstra, Keyser A, and Ongerboer de Visser, B. W., eds. Neuro-oncology: Primary tumors and neurological complications of cancer. Amsterdam: Elsevier, 1993.

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8

Montreal Neurological Hospital. Nursing Education Committee. Neuro nursing handbook: Four primary concerns: increased intracranial pressure, seizures, mobility loss, communication disorders. Edited by MacMillan Mary Irene and Robertson Caroline. [Montreal]: Montreal Neurological Hospital Nursing Department, 1988.

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9

Edwards, Clare M. The roles of central neural and local factors in primary Raynaud's disease. Birmingham: University of Birmingham, 1998.

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10

Der Anscheinsbeweis der Kausalität: Unter besonderer Berücksichtigung der neueren Rechtsprechung. Frankfurt am Main: P. Lang, 1994.

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11

Yao, Dongyuan. Properties of neurons in primate face motor cortex in relation to orofacial movements and influence of face primary somatosensory cortex. [Toronto: University of Toronto, Faculty of Dentistry, 2000.

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12

Ricketts, Charlene Michelle. The neural basis of the effects of aging on temporal processing in the rat primary auditory cortex. Ottawa: National Library of Canada, 1998.

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13

service), SpringerLink (Online, ed. Circuits in the Brain: A Model of Shape Processing in the Primary Visual Cortex. New York, NY: Springer-Verlag New York, 2009.

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14

Ziskind, Avi. Neurons in Cat Primary Visual Cortex cluster by degree of tuning but not by absolute spatial phase or temporal response phase. [New York, N.Y.?]: [publisher not identified], 2013.

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15

I, Van Allen Margot, McCourt Caterine, and Lee Nora, eds. Preconception health: Folic acid for the primary prevention of neural tube defects: a resource document for health professionals / Margot I. Van Allen, Catherine McCourt, Nora S. Lee. Ottawa, ON: Health Canada, 2002.

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16

A, Redburn Dianna, Pasantes-Morales Herminia, Instituto Venezolano de Investigaciónes Científicas., American Society for Neurochemistry, and International Society for Neurochemistry, eds. Extracellular and intracellular messengers in the vertebrate retina: Based primarily on the proceedings of a satellite symposium of the Instituto Venezolano de Investigaciónes Científicas (IVIC) meeting held in Caracas, Venezuela, May 1987. New York: A.R. Liss, 1989.

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17

Zenker, Wolfgang, and Winfried L. Neuhuber. Primary Afferent Neuron: A Survey of Recent Morpho-Functional Aspects. Springer London, Limited, 2012.

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18

Turner, Martin R. Motor neuron disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0232.

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Motor neuron disease (MND) is characterized by progressive muscular weakness due to simultaneous degeneration of lower and upper motor neurons (L/UMNs). Involvement of LMNs, arising from the anterior horns of the spinal cord and brainstem, leads to secondary wasting as a result of muscle denervation. Involvement of the UMNs of the motor cortex and corticospinal tract results in spasticity. In ~85% of cases, there is clear clinical involvement of both, and the condition is termed ‘amyotrophic lateral sclerosis’ (ALS; a term often used synonymously with MND). In ~13% of cases, there may be only LMN signs apparent, in which case the condition is termed ‘progressive muscular atrophy’, although such cases have a natural history that is to largely identical to that of ALS. In a very small group of patients (~2%), there are only UMN signs for at least the first 4 years, in which case the condition is termed ‘primary lateral sclerosis’; such cases have a uniformly slower progression. There is clinical, neuropathological, and genetic overlap between MND and some forms of frontotemporal dementia.
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19

Paganoni, Sabrina, and Nazem Atassi. Upper Motor Neuron Disorders Hereditary Spastic Paraplegia and Primary Lateral Sclerosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0032.

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Upper motor neuron (UMN) syndromes are a group of rare, degenerative neurological disorders that are classified as either hereditary spastic paraplegia (HSP) or primary lateral sclerosis (PLS). Our understanding of their underlying pathophysiology is unfortunately very limited and has been a significant barrier to the development of disease-modifying treatments. Recent advances in genetics and in vitro and in vivo disease modeling have provided new insights into disease mechanisms and hold the promise to lead to the future development of mechanism-based therapies.
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20

Zenker, Wolfgang. The Primary Afferent Neuron: A Survey Of Recent Morpho-Functional Aspects. Springer, 2011.

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21

(Editor), Wolfgang Zenker, and Winfried L. Neuhuber (Editor), eds. The Primary Afferent Neuron: A Survey of Recent Morpho-Functional Aspects. Springer, 1990.

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22

The Primary Afferent Neuron: A Survey of Recent Morpho-Functional Aspects. Springer, 2011.

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23

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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24

Chirimuuta, Mazviita, and Ian Gold. The Embedded Neuron, the Enactive Field? Edited by John Bickle. Oxford University Press, 2009. http://dx.doi.org/10.1093/oxfordhb/9780195304787.003.0010.

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This article examines the concept of the receptive field (RF) of visual neurons. It introduces the concept of visual RFs by discussing the classical picture of primary visual cortex (V1) physiology and discusses the psychophysics and computational vision of contrast discrimination to place the visual neurophysiology in context. It evaluates some recent data which questioned the classical conception of the RF and considers some options available for absorbing these data into visual theory.
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25

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

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The paper discussed in this chapter describes the first mapping of neurotrophin receptors in adult sensory neurons. Neurotrophins and their receptors were a particularly hot topic at the time, but the primary focus of interest had been in their role in development. In this paper, McMahon and colleagues characterized both mRNA and protein expression of the recently discovered trk receptors on defined populations of adult sensory neurons, correlating trk expression with other primary afferent projection neuron properties such as cell size and neuronal function. Furthermore, by showing clear correlations between the expression of different trk receptors and the physical and functional properties of defined primary afferent projections, the authors provided key evidence suggesting that nerve growth factor and neurotrophin-3 acted on functionally distinct populations of adult sensory neurons. This paper provided the basis for subsequent research on neurotrophin signalling and function in both the healthy and the diseased nervous system.
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26

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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27

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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28

Shaibani, Aziz. Muscle Stiffness and Cramps. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0020.

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Muscle stiffness as a nonspecific term means limited muscle mobility. Muscle and joint pain may be described as stiffness. Painful, sustained muscle cramps are usually associated with muscle stiffness. A careful history is paramount. Exercise-induced muscle cramps are usually myopathic (metabolic or mitochondrial myopathy) while resting, and nocturnal cramps are neurogenic [neuropathy, motor neuron disease (MND), etc.]. Metabolic cramps are electrically silent. Focal or generalized stiffness is typically seen in stiff person syndrome (SPS). Upper motor neuron (UMN) lesions are associated with spasticity and stiffness [hereditary spastic paraplegia (HSP), primary lateral sclerosis (PLS), myelopathies, etc.]. Painful cramps and fasciculation are important clues to peripheral nerve hyperexcitability disorder, which may also present with neuromyotonia. Not unusually, no cause is found for muscle cramps and stiffness. Symptomatic treatment frequently helps.
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29

Sprague, Jared Michael. TRPV1 Sensitization in Primary Sensory Neurons. 2014.

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30

Popper, Arthur N., Bernd Fritzsch, Alain Dabdoub, and Richard R. Fay. Primary Auditory Neurons of the Mammalian Cochlea. Springer London, Limited, 2015.

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31

Nageshwaran, Sathiji, Heather C. Wilson, Anthony Dickenson, and David Ledingham. Neuro-oncology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199664368.003.0013.

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This chapter discusses the classification and grading of primary brain tumours and their evidence-based treatment. The management of tumour complications (raised intracranial pressure and seizures) is also reviewed.
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32

Popper, Arthur N., Bernd Fritzsch, Alain Dabdoub, and Richard R. Fay. The Primary Auditory Neurons of the Mammalian Cochlea. Springer, 2016.

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33

Popper, Arthur N., Bernd Fritzsch, Alain Dabdoub, and Richard R. Fay. The Primary Auditory Neurons of the Mammalian Cochlea. Springer, 2015.

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34

Mason, Peggy. Cells of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190237493.003.0002.

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The nervous system is made up of neurons and glia that derive from neuroectoderm. Since neurons are terminally differentiated and do not divide, primary intracranial tumors do not arise from mature neurons. Tumors outside the nervous system may metastasize inside the brain or may release a substance that negatively affects brain function, termed paraneoplastic disease. Neurons receive information through synaptic inputs onto dendrites and soma and send information to other cells via a synaptic terminal. Most neurons send information to faraway locations and for this, an axon that connects the soma to synaptic terminals is required. Glial cells wrap axons in myelin, which speeds up information transfer. Axonal transport is necessary to maintain neuronal function and health across the long distances separating synaptic terminals and somata. A common mechanism of neurodegeneration arises from impairments in axonal transport that lead to protein aggregation and neuronal death.
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35

Horton, William D. Primary Objective: Neuro-Linguistic Psychology and Guerrilla Warfare. Eschaton Productions Inc., 1998.

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36

Twijnstra, A., A. Keyser, and B. W. Ongerboer De Visser. Neuro-Oncology: Primary Tumors and Neurological Complications of Cancer. Elsevier Publishing Company, 1993.

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37

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Neurology and neurosurgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0014.

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Chapter 14 covers the basic science and clinical topics relating to neurology and neurosurgery which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers the approach to the neurological Patient, neurological examination, neurological investigations, coma, acquired brain injury, encephalopathies, alcohol and the nervous system, brainstem disorders, common cranial nerve disorders, migraine, other primary headaches, secondary headache, neuro-ophthalmology, vertigo and hearing loss, seizures and epilepsy, intracranial pressure, stroke, central nervous system infections, neuro-oncology, multiple sclerosis, Parkinson disease, other movement disorders, spinal cord disorders (myelopathy), spinal nerve root disorders (radiculopathies), motor neurone disease, peripheral nerve disorders, mitochondrial disease and channelopathies, neuromuscular junction and muscle Disorders, sleep disorders, neurological disorders in pregnancy, the neurology of HIV infection, and functional neurology.
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38

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.
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39

Hubscher, Charles, Jeffrey C. Petruska, and Alexander Rabchevsky, eds. Plasticity of primary afferent neurons and sensory processing after spinal cord injury. Frontiers SA Media, 2015. http://dx.doi.org/10.3389/978-2-88919-396-7.

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40

Batchelor, Tracy, Ryo Nishikawa, Nancy Tarbell, and Michael Weller, eds. Oxford Textbook of Neuro-Oncology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.001.0001.

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The Oxford Textbook of Neuro-Oncology examines the epidemiology, pathogenesis, clinical features, and management of adult and childhood central nervous system (CNS) tumours. The book is organized according to the World Health Organization (WHO) classification of CNS tumours and includes an introductory chapter discussing the new, revised WHO classification that will be used in future editions of this textbook. The book reviews primary CNS tumours, metastatic CNS tumours, and familial tumour syndromes. Each chapter is organized according to a uniform framework, addressing epidemiology, aetiology, pathogenesis, clinical presentation, imaging, and treatment, with a focus on different treatment modalities and specific consideration of paediatric aspects, where applicable. Each chapter is authored by a multidisciplinary, international group of senior specialists representing the United States, Canada, Europe, and the Asia/Pacific region. It is written for generalists and specialists managing these various conditions. It provides an outlook on how current developments in molecular diagnostics, which have in part been integrated into the new WHO classification, may shape clinical decision-making in the future.
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41

Beninger, Richard J. Dopamine as the dependent variable. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0005.

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Dopamine as the dependent variable discusses how postmortem biochemistry, intracerebral microdialysis, electrophysiological recording, in vivo electrochemistry, and positron emission tomography studies provide compelling evidence that dopaminergic neurons are activated by primary rewarding stimuli including food and water and by numerous conditioned incentives, including money. Early in training, primary rewarding stimuli activate dopaminergic neurons. When a cue is reliably paired with a primary rewarding stimulus over trials, the dopamine response begins to be seen upon presentation of the cue and eventually is not seen upon presentation of the primary rewarding stimulus when it follows the cue. These conditioned cues acquire the ability to act as rewarding stimuli that can produce incentive learning. If conditioned incentive stimuli are repeatedly presented in the absence of primary incentive stimuli, they gradually lose their ability to elicit approach and other responses and to act as rewarding stimuli by producing incentive learning in their own right.
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42

Whitaker, Leslie R., and Bruce T. Hope. Neural Mechanisms of Addiction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0177.

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Addiction is a behavior characterized by compulsive seeking and taking of drugs despite severe negative consequences. Goal-directed behaviors and the motivation to perform these behaviors are altered in human addicts so that obtaining and using addictive drugs becomes the primary and overwhelming focus of their behavior. These altered behaviors result from maladaptive reward learning in which associations between drugs and drug-associated stimuli become powerful and enduring factors guiding behavior. Neural mechanisms specific to learning are likely to underlie addiction. This chapter provides an overview of both types of neural mechanisms and how they may interact to produce addiction.
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43

Montgomery, Erwin B. Principles of Electrophysiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190259600.003.0003.

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In many ways, post-operative DBS programming is “prescribing electricity” in much the same sense as “prescribing medications.” The principles of pharmacokinetics and pharmacodynamics that guide the rational use of medications find parallels in DBS. Many drugs have their effect by binding to ligand-gated channels, particularly channels that control the flow of electrical charges, in the form of ions across the cell membrane of the neuron in the soma. The binding of drugs to receptors can open the receptor to approximate the normal opening by endogenous neurotransmitters, or to block the channel from opening when endogenous neurotransmitters are released. In the case of DBS, the electrical charges manipulated in the nervous system similarly affect neuronal membrane channels; however, these initially and primarily are voltage gated ionic conductance channels, which are described in detail in this chapter.
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44

Thomas, David G. T. Neuro-Oncology: Primary Malignant Brain Tumors (Johns Hopkins Series in Contemporary Medicine and Public Health). The Johns Hopkins University Press, 1990.

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45

Levin, Frank S. Macroscopic Manifestations of Quantum Mechanics. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198808275.003.0013.

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Some possibly unexpected macroscopic manifestations of quantum mechanics are described in Chapter 12. The first is a laser, a device both man-made and one that relies on phase effects to achieve its potent beam. How this is done is illustrated by a diagram. The next is an estimate of the maximum height of a mountain, whose result was originally shown to rely on quantum mechanics. That result, approximately 30 km, is followed by showing that white dwarf and neutron stars are each gigantic manifestations of the Pauli Exclusion Principle, the first mainly consisting of carbon nuclei and electrons, the second mainly of neutrons. In each case, the primary constituent is a fermion, whose quantum behavior is governed by the Exclusion Principle. Along the way to showing this is a review of stellar evolution and energy sources. The final example is the first quantum machine, which is barely macroscopic.
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46

Jr, William D. Willis, and Richard E. Coggeshall. Sensory Mechanisms of the Spinal Cord: Volume 1 Primary Afferent Neurons and the Spinal Dorsal Horn. Springer, 2012.

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47

Jr, William D. Willis, and Richard E. Coggeshall. Sensory Mechanisms of the Spinal Cord: Volume 1: Primary Afferent Neurons and the Spinal Dorsal Horn. 3rd ed. Springer, 2004.

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48

Jr, William D. Willis, and Richard E. Coggeshall. Sensory Mechanisms of the Spinal Cord: Volume 1 Primary Afferent Neurons and the Spinal Dorsal Horn. Springer London, Limited, 2012.

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49

Functional Neural Transplantation III - Primary and Stem Cell Therapies for Brain Repair, Part I. Elsevier, 2012. http://dx.doi.org/10.1016/c2011-0-06163-x.

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50

Functional Neural Transplantation III - Primary and Stem Cell Therapies for Brain Repair, Part II. Elsevier, 2012. http://dx.doi.org/10.1016/c2011-0-06164-1.

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