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Journal ArticleDOI

Direct evidence for an axonal site of action of capsaicin.

Jancśo G, +2 more
- 01 Aug 1980 - 
- Vol. 313, Iss: 1, pp 91-94
TLDR
It is suggested that local capsaicin treatment of peripheral nerves selectively damages the chemosensitive nerve fibres presumably by depleting their substance P content.
Abstract
1. Local application of capsaicin to the sciatic nerve of rats induced a long-lasting increase in the nociceptive threshold as tested by the hot-plate method, and prevented neurogenic inflammation in the lateral part of the dorsal skin of the rat's paw. 2. Application of capsaicin to the saphenous nerve prevented the neurogenic inflammatory response, induced either by antidromic electrical stimulation of the saphenous nerve or by painting the skin with mustard oil, in the medial part of the dorsal skin of the paw. 3. The functional impairment induced by local capsaicin treatment of saphenous or sciatic nerves was strictly confined to the skin area supplied by the corresponding nerve. 4. It is suggested that local capsaicin treatment of peripheral nerves selectively damages the chemosensitive nerve fibres presumably by depleting their substance P content.

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Citations
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Journal ArticleDOI

The sensory-efferent function of capsaicin-sensitive sensory neurons

TL;DR: Development of drugs capable of controlling the sensory-efferent functions of the capsaicin-sensitive sensory neurons represent a new and very promising area of research for pharmacological treatment of various human diseases.
Journal ArticleDOI

Asthma as an axon reflex

Peter J. Barnes
- 01 Feb 1986 - 
TL;DR: In asthma, damage to airway epithelium, possibly caused by eosinophil products, exposes C-fibre afferent nerve endings and Stimulation of these endings by inflammatory mediators may result in an axon (local) reflex, which could account for at least some of the pathophysiology of asthma and this concept might lead to new strategies for treatment.
Journal ArticleDOI

Capsaicin and sensory neurones--a review.

TL;DR: This review was written as a result of a meeting on capsaicin in November 1981 at the Medical Research Council in London, where neuroscientists of different disciplines who had used capsicin in their research or studied its mode of action came together to discuss problems.
Journal ArticleDOI

Sympathetic and sensory innervation of brown adipose tissue

TL;DR: The recent recognition of BAT in normal adult humans suggests a potential target for stimulation of energy expenditure by BAT to help mitigate increased body fat storage.
References
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Journal ArticleDOI

Pharmacologically induced selective degeneration of chemosensitive primary sensory neurones

TL;DR: It is reported here that selective degeneration of neurones with a highly specific function can be produced by chemical agents in the somatosensory system as well.
Journal ArticleDOI

Substance P as neurogenic mediator of antidromic vasodilation and neurogenic plasma extravasation

TL;DR: It is concluded that vasodilation and plasma extravasation following antidromic stimulation of sensory nerves are initiated by peripheral release of substance P from chemosensitive pain fibres.
Journal ArticleDOI

Experimental immunohistochemical studies on the localization and distribution of substance P in cat primary sensory neurons.

TL;DR: The present results give strong evidence for the occurrence of SP in a certain population of primary sensory neurons and support earlier findings that SP may act as a transmitter or modulator in these neurons.
Journal ArticleDOI

Capsaicin-induced depletion of substance P from primary sensory neurones.

TL;DR: Observations strongly support the concept that substance P acts as a primary sensory transmitter and the administration of capsaicin, which is known to desensitize peripheral receptors responding to painful chemogenic stimuli, virtually abolishes the fluoride-resistant acid phosphatase activity of the substantia gelatinosa.
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