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Journal ArticleDOI

Molecular mechanisms of nociception

David Julius, +1 more
- 13 Sep 2001 - 
- Vol. 413, Iss: 6852, pp 203-210
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TLDR
Efforts to determine how primary sensory neurons detect pain-producing stimuli of a thermal, mechanical or chemical nature have revealed new signalling mechanisms and brought us closer to understanding the molecular events that facilitate transitions from acute to persistent pain.
Abstract
The sensation of pain alerts us to real or impending injury and triggers appropriate protective responses. Unfortunately, pain often outlives its usefulness as a warning system and instead becomes chronic and debilitating. This transition to a chronic phase involves changes within the spinal cord and brain, but there is also remarkable modulation where pain messages are initiated - at the level of the primary sensory neuron. Efforts to determine how these neurons detect pain-producing stimuli of a thermal, mechanical or chemical nature have revealed new signalling mechanisms and brought us closer to understanding the molecular events that facilitate transitions from acute to persistent pain.

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Citations
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Origin and Physiological Roles of Inflammation

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Cellular and Molecular Mechanisms of Pain

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Persistent postsurgical pain: risk factors and prevention

TL;DR: Strategies for identification of patients at risk and for prevention and possible treatment of this important entity of chronic pain are outlined.
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Identification of a cold receptor reveals a general role for TRP channels in thermosensation

TL;DR: These findings, together with the previous identification of the heat-sensitive channels VR1 and VRL-1, demonstrate that TRP channels detect temperatures over a wide range and are the principal sensors of thermal stimuli in the mammalian peripheral nervous system.
Journal ArticleDOI

A TRP Channel that Senses Cold Stimuli and Menthol

TL;DR: This work describes the cloning and characterization of TRPM8, a distant relative of VR1 that is specifically expressed in a subset of pain- and temperature-sensing neurons and implicates an expanded role for this family of ion channels in somatic sensory detection.
References
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Journal ArticleDOI

The capsaicin receptor: a heat-activated ion channel in the pain pathway

TL;DR: The cloned capsaicin receptor is also activated by increases in temperature in the noxious range, suggesting that it functions as a transducer of painful thermal stimuli in vivo.
Book

The Integrative Action of the Nervous System

TL;DR: In this article, the Integrative Action of the Nervous System [1906] Charles S. Sherrington, W.B. Hadden, and W.A. Baly have been discussed.
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Neuronal plasticity: increasing the gain in pain.

TL;DR: Here, a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain is developed, identifying distinct forms of Plasticity, which are term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity.
Journal ArticleDOI

Impaired Nociception and Pain Sensation in Mice Lacking the Capsaicin Receptor

TL;DR: Sensory neurons from mice lacking VR1 are severely deficient in their responses to each of these noxious stimuli and are impaired in the detection of painful heat, and showed little thermal hypersensitivity in the setting of inflammation.
Journal ArticleDOI

Textbook of pain

Patrick D. Wall, +1 more
- 01 Mar 1990 - 
TL;DR: Part 1 Basic aspects: peripheral - peripheral neural mechnaisms of nociception, the course and termination of primary afferent fibres, teh pathophysiology of damaged peripheral nerves, functional chemistry ofPrimary afferent neurons central - the dorsal horn.
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