Literature DB >> 19342617

Models and mechanisms of hyperalgesia and allodynia.

Jürgen Sandkühler1.   

Abstract

Hyperalgesia and allodynia are frequent symptoms of disease and may be useful adaptations to protect vulnerable tissues. Both may, however, also emerge as diseases in their own right. Considerable progress has been made in developing clinically relevant animal models for identifying the most significant underlying mechanisms. This review deals with experimental models that are currently used to measure (sect. II) or to induce (sect. III) hyperalgesia and allodynia in animals. Induction and expression of hyperalgesia and allodynia are context sensitive. This is discussed in section IV. Neuronal and nonneuronal cell populations have been identified that are indispensable for the induction and/or the expression of hyperalgesia and allodynia as summarized in section V. This review focuses on highly topical spinal mechanisms of hyperalgesia and allodynia including intrinsic and synaptic plasticity, the modulation of inhibitory control (sect. VI), and neuroimmune interactions (sect. VII). The scientific use of language improves also in the field of pain research. Refined definitions of some technical terms including the new definitions of hyperalgesia and allodynia by the International Association for the Study of Pain are illustrated and annotated in section I.

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Year:  2009        PMID: 19342617     DOI: 10.1152/physrev.00025.2008

Source DB:  PubMed          Journal:  Physiol Rev        ISSN: 0031-9333            Impact factor:   37.312


  320 in total

Review 1.  Pokes, sunburn, and hot sauce: Drosophila as an emerging model for the biology of nociception.

Authors:  Seol Hee Im; Michael J Galko
Journal:  Dev Dyn       Date:  2011-09-19       Impact factor: 3.780

2.  Heterosynaptic long-term potentiation at GABAergic synapses of spinal lamina I neurons.

Authors:  Henning Fenselau; Bernhard Heinke; Jürgen Sandkühler
Journal:  J Neurosci       Date:  2011-11-30       Impact factor: 6.167

Review 3.  Nociceptors: the sensors of the pain pathway.

Authors:  Adrienne E Dubin; Ardem Patapoutian
Journal:  J Clin Invest       Date:  2010-11-01       Impact factor: 14.808

Review 4.  Glutamate receptor phosphorylation and trafficking in pain plasticity in spinal cord dorsal horn.

Authors:  Xue Jun Liu; Michael W Salter
Journal:  Eur J Neurosci       Date:  2010-07-11       Impact factor: 3.386

Review 5.  [Pseudo-radicular referred leg pain].

Authors:  W von Heymann
Journal:  Schmerz       Date:  2015-12       Impact factor: 1.107

Review 6.  Current understanding of the neuropathophysiology of pain in chronic pancreatitis.

Authors:  Amporn Atsawarungruangkit; Supot Pongprasobchai
Journal:  World J Gastrointest Pathophysiol       Date:  2015-11-15

Review 7.  Neurogenic neuroinflammation: inflammatory CNS reactions in response to neuronal activity.

Authors:  Dimitris N Xanthos; Jürgen Sandkühler
Journal:  Nat Rev Neurosci       Date:  2013-11-27       Impact factor: 34.870

8.  Ionic plasticity and pain: The loss of descending serotonergic fibers after spinal cord injury transforms how GABA affects pain.

Authors:  Yung-Jen Huang; James W Grau
Journal:  Exp Neurol       Date:  2018-05-02       Impact factor: 5.330

9.  TNF-α/TNFR1 signaling is required for the development and function of primary nociceptors.

Authors:  Michael A Wheeler; Danielle L Heffner; Suemin Kim; Sarah M Espy; Anthony J Spano; Corey L Cleland; Christopher D Deppmann
Journal:  Neuron       Date:  2014-05-07       Impact factor: 17.173

Review 10.  Neuropathic Pain: Central vs. Peripheral Mechanisms.

Authors:  Kathleen Meacham; Andrew Shepherd; Durga P Mohapatra; Simon Haroutounian
Journal:  Curr Pain Headache Rep       Date:  2017-06
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