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Books on the topic 'Inhibitory Neurons'

Author: Grafiati

Published: 6 September 2023

Last updated: 26 July 2025

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1

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

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2

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

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3

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

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4

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

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5

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

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6

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 (GA

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7

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

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8

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 m

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9

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 ch

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10

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 disea

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11

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 function

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12

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

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13

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

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14

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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15

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

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16

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 inhibit

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17

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-to

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18

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 neuromodula

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19

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. m

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20

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

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Abstract Unverricht-Lundborg disease (ULD; EPM1) is an inherited neurodegenerative disorder characterized by onset at 6–15 years, stimulus-sensitive, action-activated myoclonus, epilepsy, and progressive neurological deterioration. It is caused by biallelic pathogenic variants in the CSTB gene, encoding a cystatin B. The most common of these is an unstable expansion of a dodecamer repeat element in the promoter region of the gene, leading to marked downregulation of CSTB expression. Total loss of CSTB is associated with severe neonatal-onset encephalopathy. A cystatin B–deficient mouse models

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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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