Relationships between permeable vessels, nerves, and mast cells in rat cutaneous neurogenic inflammation

1990 ◽  
Vol 68 (6) ◽  
pp. 2305-2311 ◽  
Author(s):  
J. N. Baraniuk ◽  
M. L. Kowalski ◽  
M. A. Kaliner

Electrical stimulation of rat sensory nerves produces cutaneous vasodilation and plasma protein extravasation, a phenomenon termed “neurogenic inflammation”. Rat skin on the dorsum of the paw developed neurogenic inflammation after electrical stimulation of the saphenous nerve. In tissue sections, the extravasation of the supravital dye monastral blue B identified permeable vessels. Mast cells were identified by toluidine blue stain. Permeable vessels were significantly more dense in the superficial 120 microns of the dermis than in the deeper dermis, whereas mast cells were significantly more frequent in the deeper dermis. The relationships between nociceptive sensory nerve fibers, permeable vessels, and mast cells were examined by indirect immunohistochemistry for calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and substance P (SP). CGRP-, NKA-, and SP-containing nerves densely innervated the superficial dermis and appeared to innervate the vessels that became permeable during neurogenic inflammation. In contrast, mast cells were not associated with either permeable vessels or nerve fibers. These data suggest that electrical stimulation of rat sensory nerves produces vascular permeability by inducing the release of neuropeptides that may directly stimulate the superficial vascular bed. Mast cells may not be involved in this stage of cutaneous neurogenic inflammation in rat skin.

Author(s):  
Dominika Kwiatkowska ◽  
Adam Reich

Pruritus can be defined as an unpleasant sensation that evokes a desire to scratch and significantly impairs patients’ quality of life. Pruritus is widely observed in many dermatoses, including mastocytosis, a rare disease characterized by abnormal accumulation of mast cells, which can involve skin, bone marrow, and other organs. Increasing evidence highlights the role of mast cells in neurogenic inflammation and itching. Mast cells release various pruritogenic mediators, initiating subsequent mutual communication with specific nociceptors on sensory nerve fibres. Among important mediators released by mast cells that induce pruritus, one can distinguish histamine, serotonin, proteases, as well as various cytokines. During neuronal-induced inflammation, mast cells may respond to numerous mediators, including neuropeptides, such as substance P, neurokinin A, calcitonin gene-related peptide, endothelin 1, and nerve growth factor. Currently, treatment of pruritus in mastocytosis is focused on alleviating the effects of mediators secreted by mast cells. However, a deeper understanding of the intricacies of the neurobiology of this disease could help to provide better treatment options for patients.


1995 ◽  
Vol 73 (7) ◽  
pp. 908-914 ◽  
Author(s):  
Jan M. Lundberg

Tachykinin peptides, substance P (SP) and neurokinin A (NKA), are released from airway sensory nerves upon exposure to irritant chemicals and endogenous agents including bradykinin, prostaglandins, histamine, and protons. The released neuropeptides are potent inducers of a cascade of responses, including vasodilatation, mucus secretion, plasma protein extravasation, leukocyte adhesion–activation, and bronchoconstriction. Neurokinin 1 receptors (preferably activated by SP) seem to be most important for inflammatory actions, while neurokinin 2 receptors (preferably activated by NKA) mediate bronchoconstriction. Species differences exist whereby rat and guinea-pig have a more developed neurogenic inflammation response than normal human airways. However, disease states such as inflammation or viral infections lead to enhanced peptide synthesis and (or) increased sensory nerve excitability. Together with increased neurokinin 1 receptor synthesis and loss of major tachykinin-degrading enzymes such as neutral endopeptidase in airway inflammation, this suggests that recently developed, orally active nonpeptide neurokinin receptor antagonists could have a therapeutic potential in asthmatic patients.Key words: neurokinins, sensory nerves, inflammation, bronchoconstriction, receptors.


Cephalalgia ◽  
1988 ◽  
Vol 8 (2) ◽  
pp. 83-91 ◽  
Author(s):  
Stephen Markowitz ◽  
Kiyoshi Saito ◽  
Michael A Moskowitz

C-fiber- dependent neurogenic plasma extravasation developed in the dura mater but not the brain after electric stimulation of the rat trigeminal ganglion or after chemical stimulation of perivascular axons with intravenous capsaicin, a drug that depolarizes sensory nerve fibers. C-fiber- independent extravasation also developed in this tissue after intravenous injections of substance P or neurokinin A (two constituents of unmyelinated C fibers) and after serotonin, bradykinin, or allergic challenge in presensitized animals. Intravenous dihydroergotamine or ergotamine tartrate, in doses similar to those used to treat migraine and cluster headache, prevented the stimulation-induced leakage of plasma proteins within the dura mater. Not unexpectedly, the acute administration of methysergide, a drug effective in the prophylactic treatment of headache, was inactive in this acute model. Neither acute nor chronic administration of propranolol affected stimulation-induced leakage of plasma protein. These results demonstrate that neurogenic inflammation develops within the dura mater in the rat and that ergot alkaloids prevent the process by a C-fiber-dependent mechanism.


Physiology ◽  
2001 ◽  
Vol 16 (1) ◽  
pp. 33-37 ◽  
Author(s):  
M. Schmelz ◽  
L. J. Petersen

The combination of vasodilation and protein extravasation following activation of nociceptors has been termed “neurogenic inflammation.” In contrast to rodents, no neurogenic protein extravasation can be elicited in healthy human skin. Dermal microdialysis has considerably increased our knowledge about neurogenic inflammation in human skin, including the involvement of mast cells.


Neuroscience ◽  
1997 ◽  
Vol 77 (3) ◽  
pp. 829-839 ◽  
Author(s):  
V Dimitriadou ◽  
A Rouleau ◽  
M.D Trung Tuong ◽  
G.J.F Newlands ◽  
H.R.P Miller ◽  
...  

2003 ◽  
Vol 95 (2) ◽  
pp. 577-583 ◽  
Author(s):  
Jianhua Li ◽  
Nicholas C. King ◽  
Lawrence I. Sinoway

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.


2001 ◽  
Vol 204 (13) ◽  
pp. 2265-2275 ◽  
Author(s):  
Michael Gebhardt ◽  
Hans-Willi Honegger

SUMMARY We investigated five different descending brain interneurons with dendritic arborizations in the deutocerebrum in the crickets Gryllus bimaculatus and G. campestris. These interneurones convey specific antennal mechanosensory information to the ventral nerve cord and all responded to forced antennal movements. These interneurones coded for velocity and showed preferences for distinct sectors of the total range of antennal movements. Their axons descended into the posterior connective either ipsilateral or contalateral to the cell body. Electrical stimulation of sensory nerves indicated that the interneurons received input from different afferents of the two antennal base segments. One interneuron had a particularly large axon with a conduction velocity of 4.4ms−1. This was the only one of the five interneurons that also received visual input. Its activity was reduced during voluntary antennal movements. The reduction in activity occurred even after de-efferentation of the antenna, indicating that it had a central origin. Although we do not have experimental evidence for behavioural roles for the descending antennal mechanosensory interneurons, the properties described here suggest an involvement in the perception of objects in the path of the cricket.


1990 ◽  
Vol 148 (1) ◽  
pp. 113-128 ◽  
Author(s):  
U. W. E. MÜLLER ◽  
FRANÇOIS CLARAC

1. The effects of cyclic electrical stimulation of the dactyl sensory nerve (DN) on the walking pattern of rock lobsters were examined at the two crucial points within the step cycle: the anterior extreme position (AEP) and the posterior extreme position (PEP). 2. Stimulation during the occurrence of the PEP affected neither the movement pattern of the stimulated leg itself nor that of the ipsilateral adjacent legs. 3. Stimulation of the same intensity during the occurrence of the AEP interrupted the oscillation of the stimulated leg and affected the phase relationships of the ipsilateral adjacent legs. 4. The possibility that indirect influences were mediated by coupling to the substratum can be excluded. Neuronal connections may therefore exist between the funnel canal organs (FCO) of a single leg and the motor output of the adjacent legs. The discussion deals with whether the described channels alone are able to fulfil the requirements of a ‘coordinating mechanism’ as described in the literature.


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