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Books on the topic 'Inhibitory Neurons'

Author: Grafiati

Published: 6 September 2023

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1

Developmental plasticity of inhibitory circuitry. New York: Springer, 2010.

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2

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

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3

Pallas, Sarah L. Developmental Plasticity of Inhibitory Circuitry. Springer, 2014.

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4

Saraga, Fernanda. Use of compartmental models to predict physiological properties of hippocampal inhibitory neurons. 2006.

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5

GABA(A) receptors that mediate a tonic inhibitory current in hippocampal neurons: Modulation by antagonists and anti-convulsants. Ottawa: National Library of Canada, 2002.

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6

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.

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7

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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8

Mather, George. Two-Stroke Apparent Motion. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199794607.003.0073.

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“Two-stroke” apparent motion is a powerful illusion of directional motion generated by alternating just two animation frames, which occurs when a brief blank interframe interval is inserted at alternate frame transitions. This chapter discusses this illusion, which can be explained in terms of the receptive field properties of motion-sensing neurons in the human visual system. The temporal response of these neurons contains both an excitatory phase and an inhibitory phase; when the timing of the interframe interval just matches the switch in response sign, the illusion occurs. Concepts covered in this chapter include four-stroke as well as two-stroke apparent motion, motion aftereffect, and motion detection.

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9

Schaible, Hans-Georg, and Rainer H. Straub. Pain neurophysiology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0059.

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Physiological pain is evoked by intense (noxious) stimuli acting on healthy tissue functioning as a warning signal to avoid damage of the tissue. In contrast, pathophysiological pain is present in the course of disease, and it is often elicited by low-intensity stimulation or occurs even as resting pain. Causes of pathophysiological pain are either inflammation or injury causing pathophysiological nociceptive pain or damage to nerve cells evoking neuropathic pain. The major peripheral neuronal mechanism of pathophysiological nociceptive pain is the sensitization of peripheral nociceptors for mechanical, thermal and chemical stimuli; the major peripheral mechanism of neuropathic pain is the generation of ectopic discharges in injured nerve fibres. These phenomena are created by changes of ion channels in the neurons, e.g. by the influence of inflammatory mediators or growth factors. Both peripheral sensitization and ectopic discharges can evoke the development of hyperexcitability of central nociceptive pathways, called central sensitization, which amplifies the nociceptive processing. Central sensitization is caused by changes of the synaptic processing, in which glial cell activation also plays an important role. Endogenous inhibitory neuronal systems may reduce pain but some types of pain are characterized by the loss of inhibitory neural function. In addition to their role in pain generation, nociceptive afferents and the spinal cord can further enhance the inflammatory process by the release of neuropeptides into the innervated tissue and by activation of sympathetic efferent fibres. However, in inflamed tissue the innervation is remodelled by repellent factors, in particular with a loss of sympathetic nerve fibres.

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10

Stafstrom, Carl E. Disorders Caused by Botulinum Toxin and Tetanus Toxin. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0156.

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Anaerobic organisms of the genus Clostridia (C) can cause significant human disease. Exotoxins secreted by C botulinum and C tetani cause botulism and tetanus, respectively (summarized in Table 156.1). Botulinum neurotoxin causes neuromuscular blockade by interfering with vesicular acetylcholine release, leading to cholinergic blockade at the neuromuscular junctions of skeletal muscle, and consequently, symmetric flaccid paralysis. Tetanus toxin prevents release of inhibitory neurotransmitters at central synapses, leading to overactivity of motor neurons and muscle rigidity and spasms. This chapter reviews clinical features of botulism and tetanus and discusses their pathophysiological basis.

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11

Sandkühler, Jürgen. Making the link from “central sensitization” to clinical pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0047.

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The landmark paper discussed in this chapter is ‘Central sensitization: Implications for the diagnosis and treatment of pain’, published by C. J. Woolf in 2011. The phrase ‘central sensitization’ is often used as an umbrella term for all kinds of central nervous system (CNS) mechanisms contributing to pain hypersensitivity. The International Association for the Study of Pain (IASP) defines ‘central sensitization’ as the ‘increased responsiveness of nociceptive neurons in the CNS’. In the CNS, highly distinct mechanisms contribute to pain hypersensitivity depending upon pain aetiology and disease stage. These include modification of synaptic strength, inhibitory tone, and membrane excitability and often involve components of neuroinflammation. It is thus recommended to avoid using the phrase ‘central sensitization’ in the scientific literature all together and replace it with unambiguous technical terms such as ‘CNS mechanisms of pain hypersensitivity’ or with the specific mechanism(s) and CNS location(s) in mind.

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12

Gaetz, Michael B., and Kelly J. Jantzen. Electroencephalography. Edited by Ruben Echemendia and Grant L. Iverson. Oxford University Press, 2016. http://dx.doi.org/10.1093/oxfordhb/9780199896585.013.006.

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Axonal injury is currently considered to be the structural substrate behind most concussion-related neurological dysfunction. Because the principal generators of EEG fields are graded excitatory and inhibitory synaptic potentials of pyramidal neurons, the EEG is well suited for characterizing large-scale functional disruptions associated with concussion induced metabolic and neurochemical changes, and for connecting those disruptions to deficits in behavior and cognition. This essay provides an overview of the use of EEG and newly developed analytical procedures for the measurement of functional impairment related to sport concussion. Elevations in delta and theta activity can be expected in a percentage of athletes and change in asymmetry and coherence may also be present. Newer techniques are likely to be of critical importance for understanding the anatomical and physiological basis of cognitive deficits and may provide additional insight into susceptibility to future injury. Computational modeling may advance our understanding of concussion.

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13

Kerlin, Aaron Michael. Response properties of inhibitory neuron subtypes in mouse visual cortex. 2011.

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14

Lee, David WK. Dopamine-induced Gbetagamma-mediated inhibitory pathways in vesicle release in an identified respiratory Lymnaea neuron. 2007.

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15

Cavanna, Andrea E. Antiepileptic drugs and behaviour: mechanisms of action. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198791577.003.0002.

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Antiepileptic drugs (AEDs) exert their pharmacological properties on both epileptic seizures and behaviour through different mechanisms of action. These include modulation of ion (mainly sodium and calcium) conductance through voltage-gated channels located within the neuronal membrane, as well as facilitation of inhibitory (GABAergic) neurotransmission and inhibition of excitatory (glutamatergic) neurotransmission, resulting in regulation of neuronal excitability.

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16

Modulation of oscillatory activity in inhibitory neuronal networks by anesthetics: The role of receptor desensitization. Ottawa: National Library of Canada, 2001.

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17

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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18

Fomberstein, Kenneth, Marissa Rubin, Dipan Patel, John-Paul Sara, and Abhishek Gupta. Perioperative Opioid Analgesics of Use in Pain Management for Spine Surgery. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626761.003.0004.

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This chapter compares the basic properties of several opioid analgesics and explores their applications in perioperative pain control in spine surgery. Parenteral opioids have long been the cornerstone of treatment for postoperative pain; they work by inhibiting voltage-gated calcium channels and increasing potassium influx, which results in reduced neuronal excitability, thereby inhibiting the ascending transmission of painful stimuli and activating the descending inhibitory pathways. This chapter reviews concepts including opioid conversion and rotation, opioid tolerance, and opioid cross-tolerance. It discusses common opioid side effects, and it explores the perioperative use of several specific opioids including remifentanil, sufentanil, methadone, oxycodone, morphine, and tapentadol and discusses their use in spine surgery. Additionally, this chapter discusses patient-controlled analgesia (PCA) and its importance in postoperative pain control.

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19

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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20

Krueger, Darcy A., and Jamie Capal. Familial CNS Tumor Syndromes. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0136.

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Tuberous sclerosis complex is an autosomal dominant multi-system disease that involves the skin, brain, heart, lungs, and kidneys and is associated with seizures including infantile spasms, intellectual disability, autism and pulmonary and heart disease. Skin lesions can be particularly disfiguring and infantile spasms can be associated with marked cognitive decline. The outlook for patients has improved markedly with the recognition that TSC is caused by upregulation of the mammalian target of rapamycin (mTOR) enzyme, which connects energy needs and supply with cellular and neuronal growth. mTOR is upregulated in TSC because of mutations in hamartin or tuberin, which normally serve as a brake on mTOR. The drug rapamycin is commonly used as an immunosuppressive for patients undergoing kidney transplants; it has also found a new use in patients with TSC. Although the drug is immunosuppressive for non-TSC patients, careful titration of the drug in TSC patients corrects its upregulation but is not particulary immunosuppressive. Additional mTOR inhibitors such as everolimus have been developed and have been shown to be effective for pulmonary disease associated with TSC. Rapamycin in ointment form is dramatically effective in suppressing skin lesions of TSC and studies are underway to test the effect of mTOR inhibitors on seizures, brain tubers, intellect, and features of autism. Infantile spasms associated with TSC are very responsive to vigabatrin.

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21

(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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