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PubMed2006

[Experimental study on the mechanisms of regulating airway neurogenic inflammation in asthma by never growth factor and leukemia inhibitory factor].

OBJECTIVE: To study the mechanisms of regulating airway neurogenic inflammation in asthma by never growth factor (NGF) and leukemia inhibitory factor (LIF), and then to explore new targets in treating asthma. METHODS: Adult male SD rats (n 36) were divided into the normal group, the asthmatic group and the anti-NGF group at random. There were 12 rats in each group. The asthma models were established by sensitization and challenge with ovalbumin, and the asthma model was treated with anti-NGF. The expression of NGF, LIF and substance P (SP) in lung tissue or in doral root ganglion of each rat were detected by immunohistochemistry and hybridisation in situ. RESULTS: (1) The gray-levels of NGF protein/NGF mRNA, LIF protein/LIF mRNA in the lungs were 157 +/- 7, 138 +/- 8, 156 +/- 6, 141 +/- 10 for the asthmatic group respectively, 183 +/- 7, 190 +/- 7, 187 +/- 7, 181 +/- 8 for the normal control group respectively, and 177 +/- 6, 169 +/- 9, 178 +/- 7, 172 +/- 9 for the asthmatic group with anti-NGF treatment. There were significant differences in gray-level of NGF protein/NGF mRNA, LIF protein/LIF mRNA among those three groups (t = 19.40, 15.80, 20.38, [corrected] 14.79, all P < 0.01). (2) The gray-levels of NGF protein/LIF protein, SP protein/SP mRNA in the doral root ganglions were 136 +/- 8, 148 +/- 6, 140 +/- 8, 128 +/- 8 for the asthmatic group respectively, 185 +/- 7, 187 +/- 8, 174 +/- 7, 180 +/- 8 for the normal control group respectively, and 164 +/- 6, 170 +/- 8, 163 +/- 9, 157 +/- 7 for the asthmatic group with anti-NGF treatment. There were also significant differences in gray-level of NGF protein/LIF protein, SP protein/SP mRNA among those three groups (t = 29.50, 22.65, 23.12, 28.71, all P < 0.01). CONCLUSION: Enhancing the synthesis and release of SP in doral root ganglion may be one of the mechanisms by which NGF and LIF regulate airway neurogenic inflammation in asthmatic rats, and this mechanism can be depressed by the intervention of anti-NGF.

Animals↗
PubMed2004

Potentiation of sural nerve Abeta action potential after neurogenic inflammation.

Inflammatory mediators modulate voltage-gated sodium channels through protein kinase-mediated pathways. However, it is not clear whether neurogenic inflammation may also alter the properties of distantly located channels along axon shafts supplying the inflamed dermatome. In this study, localized inflammation was induced via intradermal injection of capsaicin within the receptive field of the sural nerve, and compound action potentials (CAP) evoked by sural nerve stimulation were recorded from the sciatic nerve proximally. The area measured under the A beta CAP increased significantly within 5 min after capsaicin injection. Distal injection of lidocaine at the ankle division of the sural nerve prior to capsaicin injection reversed this increase. In addition, application of a lipophilic protein kinase inhibitor H7 (100 microM) through a perfusion chamber placed on the sciatic nerve also reversed this increase. Our results suggest that during neurogenic inflammation, action potential activity is increased, triggering activation of protein kinases that may rapidly alter membrane conductance to potentiate action potential propagation along peripheral nerves.

Action Potentials↗
PubMed2001

Neurogenic inflammation and chronic pelvic pain.

Chronic pelvic pain is a puzzling disease entity. The pathophysiological mechanisms of chronic pelvic pain are not clear and current treatment strategies are often not successful, leaving patients as well as health care providers frustrated. In a subgroup of patients with chronic pelvic pain (e.g., interstitial cystitis, irritable bowel syndrome, vulvar vestibulitis, prostatodynia/prostatitis, and loin pain/hematuria syndrome) inflammatory changes are observed, for which no etiology has been identified. These inflammatory changes might be due to neurogenic inflammation. Applying the concept of neurogenic inflammation to chronic pelvic pain provides new insights into the pathophysiological mechanisms of these pain syndromes, makes it possible to account for the heterogeneity and variability observed in the clinical presentation, and might lead to the development of novel therapies.

Animals↗
PubMed2006

[Regulation effect of nerve growth factor on Ras-MAPK signal transduction pathway in neurogenic inflammation of asthma].

OBJECTIVE: To investigate the regulatory effect of nerve growth factor (NGF) on Ras-MAPK signal transduction pathway in neurogenic inflammation of asthma. METHODS: Thirty-six Sprague-Dawley rats were randomly divided into 3 groups (control group, asthma group and anti-NGF group). The asthmatic model was established by ovalbumin inhalation and injection. The protein expressions of pan-Ras, pERK and c-fos in the dorsal root ganglion and lung of the asthma group and the control group were examined by immunohischemical method. Anti-NGF antibody was used to investigate how it affected the protein expression of pan-Ras, pERK and c-fos in the dorsal root ganglion and the lung of the asthma group. PD98059 (the inhibitor of MAPK) and PMA (the enhancer of PKC) were used to culture the NHBEC. Cell extracts were analyzed for pERK, total-ERK and c-fos by Western blot. RESULTS: The protein expressions of pan-Ras, pERK and c-fos in the lung and dorsal root ganglion of the asthma group were significantly higher than those of the control group (P < 0.01). The protein expressions of pan-Ras, pERK and c-fos were decreased by the anti-NGF treatment (P < 0.01) . The expressions of epithelial pERK and c-fos in the NGF group were significantly higher than those in the control group, and PD98059 could inhibit NGF inducing NHBEC to produce pERK and c-fos. PMA could enhance the effects of NGF. CONCLUSION: NGF may play a role in the pathogenesis of neurogenic inflammation in asthma through Ras-MAPK signal transduction pathway.

Animals↗
PubMed1991

Modulation of neurogenic inflammation by neutral endopeptidase.

The enzyme neutral endopeptidase (NEP) is bound to the membranes of selected cells in the airways that have receptors for tachykinins. The location of the enzyme, along with its selectivity of substrates (tachykinins are a preferred substrate), allows the enzyme to cleave tachykinins that come close to the cell-surface receptors. By cleaving and thus inactivating tachykinins released during stimulation of the sensory nerves, NEP limits the degree of neurogenic inflammation. Neutral endopeptidase exists in the basal cells of the airway epithelium, nerves, smooth muscle, glands, blood vessels, and perhaps other cells. Thus, the enzyme modulates smooth muscle contraction, gland secretion, cough, vascular permeability, and neutrophil adhesion. Decreased NEP activity occurs with epithelial removal, during respiratory viral infections, and during exposure to irritants (e.g., cigarette smoke and toluene diisocyanate). Delivery of recombinant NEP (rNEP) by aerosol suppressed cough responses during neurogenic inflammation. We suggest that decreased NEP activity will result in exaggerated neurogenic inflammation and may play an important role in inflammatory diseases in airways. Furthermore, drugs that cause up-regulation of NEP may play a therapeutic role by suppressing neurogenic responses. Replacement therapy with rNEP may be useful in diseases where inflammatory peptides (e.g., tachykinins, bradykinin) play a role in pathogenesis.

Animals↗
PubMed2006

Effect of pituitary adenylate cyclase activating polypeptide-38 on sensory neuropeptide release and neurogenic inflammation in rats and mice.

Substance P (SP) and calcitonin gene-related peptide (CGRP), released from capsaicin-sensitive sensory nerves induce local neurogenic inflammation, while somatostatin exerts systemic anti-inflammatory actions. The aim of the present study was to investigate the release of pituitary adenylate cyclase activating polypeptide-38 (PACAP-38) and its effects on sensory neuropeptide release in vitro and acute neurogenic ear swelling in vivo. Capsaicin (10(-6) M) or electrical field stimulation (EFS; 40 V, 0.1 ms, 10 Hz, 120 s; 1200 impulses)-induced release of PACAP-38, SP, CGRP and somatostatin from isolated rat tracheae was measured with radioimmunoassay. Mustard oil-induced neurogenic inflammation in the mouse ear was determined with a micrometer and in the rat hind paw skin by the Evans Blue leakage technique. Capsaicin and EFS evoked 27% and more than twofold elevation of PACAP-38 release respectively, compared with the prestimulated basal values from isolated trachea preparation. Exogenously administered PACAP-38 (20-2000 nM) diminished both capsaicin- and EFS-evoked sensory neuropeptide release in a concentration-dependent manner. The maximal inhibitory effects of PACAP on capsaicin-induced substance P, CGRP and somatostatin release amounted to 75.4%, 73.3% and 90.0%, while EFS-evoked release of these peptides was 80.03%, 87.7% and 67.7%. In case of capsaicin stimulation the EC50 values for substance P, CGRP and somatostatin were 82.9 nM, 60.1 nM and 66.9 nM, respectively. When EFS was performed, these corresponding EC50 data were 92.1 nM, 67.8 nM and 20.9 nM. PACAP-38 (10, 100 and 1000 microg/kg i.p. in 200 microl volume) inhibited neurogenic ear swelling in the mouse. Furthermore, 100 microg/kg i.p. PACAP also significantly diminished mustard oil-evoked plasma protein extravasation in the rat skin. These results suggest that PACAP-38 is released from the stimulated peripheral terminals of capsaicin-sensitive afferents and it is able to inhibit the outflow of sensory neuropeptides. Based on this mechanism of action PACAP is also able to effectively diminish/abolish neurogenic inflammatory response in vivo after systemic administration.

Animals↗
PubMed2005

[The role of airway neurogenic inflammation in gastro-esophageal reflux induced cough].

OBJECTIVE: To investigate the role of airway neurogenic inflammation in the pathogenesis of gastro-esophageal reflux induced cough (GERC). METHODS: Sputum was induced by hypertonic saline aerosol inhalation in 20 patients with GERC (GERC group), 10 healthy subjects (normal control group) and 8 patients with chronic cough due to other causes but complicated with gastro-esophageal reflux diseases (GERD, GERD group). Airway mucosal biopsy was performed in 6 patients with GERC and 4 patients with GERD using flexible fiberoptic bronchoscopy. The expression of substance P (SP), neurokinin 1 receptor and neurokinin A (NKA) in sputum cells and airway mucosa were detected by immunohistochemistry, and was assessed semi-quantitatively. SP, NKA, and NKB in the supernatant of induced sputum were measured with enzyme linked immunosorbent assay. Calcitonin gene-related peptide (CGRP) was measured with radioimmunoassay. RESULTS: The concentration of SP in the supernatant of induced sputum was significantly higher in GERC group [(266 +/- 207) ng/L] than those in normal control group [(143 +/- 36) ng/L, P < 0.05] and GERD group [(130 +/- 11) ng/L, P < 0.05], and the sputum supernatant concentration of CGRP in GERC group [(180 +/- 83) ng/L] was significantly higher than those in normal control group [(105 +/- 64) ng/L, P < 0.01] and GERD group [(89 +/- 16) ng/L, P < 0.01]. The expression of SP, NK-1 receptor and NKA in induced sputum cells in GERC group were significantly higher than those in normal control group (P < 0.01, < 0.05, < 0.05) and GERD group (all P < 0.05); Expressions of SP in airway mucosa was significantly higher in GERC group than in GERD group (P < 0.01). After treatment, the concentration of CGRP in the supernatant of sputum in GERC patients was significantly lower than that before treatment (P < 0.05); the expression of SP, NK-1 and NKA in the induced sputum cells were significantly lower than that before treatment (P < 0.01, P < 0.01 or P < 0.05). CONCLUSION: There is airway neurogenic inflammation in GERC patients, which maybe closely related to the development of GERC.

Adult↗
PubMed2000

The tachykinin NK(1) receptor antagonist SR140333 prevents the increase of nerve growth factor in rat paw skin induced by substance P or neurogenic inflammation.

Target-derived nerve growth factor provides trophic support for adult primary afferent neurons containing calcitonin gene-related peptide and tachykinins. Noxious chemical or thermal stimuli cause the release of these mediators from peripheral afferent nerve endings. However, little is known of the extent to which these mediators, in turn, influence nerve growth factor expression in the innervated tissue. The aim of this study was therefore to investigate the possible effect of exogenous substance P, or neurogenic inflammation on the nerve growth factor concentration in the skin of the rat hindpaw. Our results show that substance P as well as topical application of mustard oil cause a significant increase in detectable nerve growth factor, an effect that was prevented by treatment of rats with the tachykinin NK(1) receptor antagonist SR140333. We did not observe a significant inhibitory effect of SR140333 on the nerve growth factor content in non-treated skin, or the nerve growth factor increase caused by carrageenan or allergic inflammation. The results provide evidence that substance P as well as neurogenic inflammation cause a rapid increase in detectable nerve growth factor in the paw skin and suggest the involvement of NK(1) receptors in this effect. We obtained no evidence for the participation of a NK(1) receptor-mediated nerve growth factor increase in models of inflammation induced by non-neurogenic stimuli.

Animals↗
PubMedDate not supplied

Sensory nerves, neurogenic inflammation and pain: missing components of alternative irritation strategies? A review and a potential strategy.

The eyes and skin are highly innervated by sensory nerves; stimulation of these nerves by irritants may give rise to neurogenic inflammation, leading to sensory irritation and pain. Few in vitro models of neurogenic inflammation have been described in conjunction with alternative skin and eye irritation methods, despite the fact that the sensory innervation of these organs is well-documented. To date, alternative approaches to the Draize skin and eye irritation tests have proved largely successful at classifying severe irritants, but are generally poor at discriminating between agents with mild to moderate irritant potential. We propose that the development of in vitro models for the prediction of sensory stimulation will assist in the re-classification of the irritant potential of agents that are under-predicted by current in vitro strategies. This review describes the range of xenobiotics known to cause inflammation and pain through the stimulation of sensory nerves, as well as the endogenous mediators and receptor types that are involved. In particular, it focuses on the vanilloid receptor, its activators and its regulation, as these receptors function as integrators of responses to numerous noxious stimuli. Cell culture models and ex vivo preparations that have the potential to serve as predictors of sensory irritation are also described. In addition, as readily available sensory neuron cell line models are few in number, stem cell lines (with the capacity to differentiate into sensory neurons) are explored. Finally, a preliminary strategy to enable assessment of whether incorporation of a sensory component will enhance the predictive power of current in vitro eye and skin testing strategies is proposed.

Animal Use Alternatives↗
PubMed1989

Changes in epithelial secretory cells and potentiation of neurogenic inflammation in the trachea of rats with respiratory tract infections.

In rats respiratory tract infections due to Sendai virus and coronavirus usually are transient, but they can have long-lasting consequences when accompanied by Mycoplasma pulmonis infections. Morphological alterations in the tracheal epithelium and a potentiation of the inflammatory response evoked by sensory nerve stimulation ("neurogenic inflammation") are evident nine weeks after the infections begin, but the extent to which these changes are present at earlier times is not known. In the present study we characterized these abnormalities in the epithelium and determined the extent to which they are present 3 and 6 weeks after the infections begin. We also determined the magnitude of the potentiation of neurogenic inflammation at these times, whether the potentiation can be reversed by glucocorticoids, and whether a proliferation of blood vessels contributes to the abnormally large amount of plasma extravasation associated with this potentiation. To this end, we studied Long-Evans rats that acquired these viral and mycoplasmal infections from other rats. We found that the tracheal epithelium of the infected rats had ten times as many Alcian blue-PAS positive mucous cells as did that of pathogen-free rats; but it contained none of the serous cells typical of pathogen-free rats, so the total number of secretory cells was not increased. In addition, the epithelium of the infected rats had three times the number of ciliated cells and had only a third of the number of globule leukocytes. In response to an injection of capsaicin (150 micrograms/kg i.v.), the tracheas of the infected rats developed an abnormally large amount of extravasation of two tracers, Evans blue dye and Monastral blue pigment, and had an abnormally large number of Monastral blue-labeled venules, particularly in regions of mucosa overlying the cartilaginous rings. This abnormally large amount of extravasation was blocked by dexamethasone (1 mg/day i.p. for 5 days). We conclude that M. pulmonis infections, exacerbated at the outset by viral infections, result within three weeks in the transformation of epithelial serous cells into mucous cells, the proliferation of ciliated cells, and the depletion of globule leukocytes. They also cause a proliferation of mediator-sensitive blood vessels in the airway mucosa, which is likely to contribute to the potentiation of neurogenic inflammation that accompanies these infections.

Animals↗
PubMed1999

Secretoneurin and neurogenic inflammation.

AIM: Review of evidence that the 33-amino-acid polypeptide secretoneurin, which is generated by proteolytic cleavage of secretogranin II, plays a role in neurogenic inflammation. METHODS: Survey of the literature using a MEDLINE search database. RESULTS: Secretoneurin is synthesized in spinal ganglia, transported through the dorsal roots and stored in the axon terminals of primary afferent neurons. Investigations using capsaicin suggest that secretoneurin functions as an excitatory transmitter. Secretoneurin specifically activates various cell functions including the chemotactic migration of monocytes, eosinophils, fibroblasts, smooth muscle cells, and endothelial cells, which suggests that the peptide may modulate inflammatory reactions. Secretoneurin receptors have been functionally characterized. They are G-proteins linked and effects are abrogated by inhibition of protein kinase C. CONCLUSION: With actions as diverse as those seen with other mediators such as tachykinins, secretoneurin may be considered another sensory neuropeptide with modulatory potential in neurogenic inflammation.

Animals↗
PubMed2001

Influence of painful chronic neuropathy on neurogenic inflammation.

The effect of topical application of capsaicin cream on neurogenic inflammation was investigated in a neuropathic pain model in rat. The neuropathic state was induced by loose ligation of the sciatic nerve with a chromic gut suture. A marked thermal hyperalgesia was observed in response to heat stimulation applied to the operated side from 3 days through 2 weeks, followed by a gradual return to the control level 35 days after surgery. In sham-operated animals, topical application of capsaicin cream to both sides of the hind paw, the instep and sole, as well as antidromic stimulation of the sciatic nerve led to a significant increase in the amounts of Evans blue and substance P (SP) released into the perfusates. This stimulus-induced extravasation was significantly suppressed by pretreatment with RP67580, an NK1 antagonist. On day 7 after ligation, capsaicin- and antidromic stimulation-induced extravasation were significantly reduced. At this time, both amount of SP released immediately after application of capsaicin and during antidromic stimulation were almost similar to that in sham-operated rats, whereas the basal amount of SP release significantly increased in ligated animals. In particular a major release of SP was detected immediately after the start of the perfusion compared with that in sham-operated rats. Plasma extravasation evoked by SP (10(-4) M) applied to the subcutaneous perfusate was significantly less in ligated than in sham-operated rats. These results suggest that nerve injury with chronic pain may produce increase in basal SP release into the peripheral tissues, and then such enhanced SP release cause reduction of SP-induced extravasation.

Administration, Topical↗
PubMed1994

[Neurogenic inflammation and area of involvement of the facial nerve of the rat].

Antidromic electrical stimulation of sensory nerves produces vascular hyperpermeability, plasma protein extravasation and oedema. The initial phase of this inflammatory reaction is induced by the release of the neuropeptides CGRP, SP and NKA; the later phase is induced by mast cells. In previous investigations we were able to show that the facial nerve of the rat contains CGRP, SP and NKA as well as mast cells. The same mechanism--increased vascular permeability--plasma extravasation--oedema--is thought to be part of the pathogenesis of Bell's palsy. Hence, we tried to produce neurogenic inflammations in the facial nerves of six adult Wistar rats. To assess plasma extravasation we used Evans blue, a dye which binds to serum albumin, according to the method described by Brokaw and White (1992). Having cut the facial nerve distal of the stylomastoid foramen we induced a neurogenic inflammation by the application of an electrical stimulus to the distal part of the nerve. In comparison to the contralateral, non-stimulated side, we recognized that the inflammatory reactions were limited to the area of the skin innervated by the posterior auricular nerve. So far, we can transfer this "neurogenic inflammation model" the well-known relationship between nerves and inflammatory reactions to this limited area innervated by the facial nerve.

Animals↗
PubMed2003

Neurogenic inflammation in primary headaches.

The headache in migraine is thought to result from neuronal nociceptive activity in the trigeminovascular system, that is, the meninges. In addition, trigeminal axons projecting to the meninges contain vasoactive neuropeptides, such as substance P, calcitonin gene-related peptide and neurokinin A, that may promote, when released, plasma protein leakage and vasodilation within dura mater, characteristic of neurogenic inflammation. Thus, it has been hypothesized that a sterile neurogenic inflammation in the meninges may be involved in generating or sustaining, via occurrence of a vicious cycle, the pain accompanying the migraine attacks. We here review the evidence in support of this hypothesis as well as its potential significance in better tailoring therapies in migraine or other types of primary headaches.

Animals↗
PubMed1995

The in vivo pharmacological profile of a 5-HT1 receptor agonist, CP-122,288, a selective inhibitor of neurogenic inflammation.

1. The aim of the present study was to investigate the in vivo pharmacological profile of CP-122,288, an indole-derivative with a conformationally restricted N-methylpyrrolidinyl basic side chain in the C-3 position. This C-3 substituent structurally differentiates CP-122,288 from the 5-HT1D receptor agonist sumatriptan, which possesses an N,N-dimethylaminoethyl group. [Formula: see text] 2. When administered prior to electrical stimulation of the trigeminal ganglion, CP-122,288 (0.3-300 ng kg-1, i.v.) produced a dose-related inhibition of plasma protein extravasation in rat dura mater (minimum effective dose, MED, 3 ng kg-1 i.v., P < 0.05; maximal inhibition of plasma extravasation at 30 ng kg-1 i.v., P < 0.01). Sumatriptan produced a similar inhibition of plasma leakage in the dura, but at much higher dose levels (MED, 100 micrograms kg-1 i.v., P < 0.05). Thus, CP-122,288 is of the order of 10(4) fold more potent than sumatriptan. 3. At all doses tested, CP-122,288 did not inhibit plasma protein extravasation measured in extracranial tissues such as the lower lip, eyelid, and conjunctiva. 4. In a separate series of studies in the anaesthetized rat, CP-122,288 (0.003-3 micrograms kg-1 i.v.) produced no change in either heart rate or mean arterial blood pressure, thus demonstrating that doses of CP-122,288 which inhibit plasma protein leakage in rat dura, are devoid of hemodynamic effects. 5. Following a 5 min period of electrical stimulation of the trigeminal ganglion, a 20 min period of sustained neurogenically-driven plasma extravasation, occurring in the absence of electrical stimulation, was initiated. By administration of the compound 5 min after completing the phase of electrical stimulation, this protocol permitted the evaluation of the activity of CP-122,288 on an ongoing and established inflammatory event. CP-122,288 (30 and 300 ng kg-1, i.v., P < 0.01 and P < 0.05, respectively) produced a complete inhibition of plasma protein leakage which was consistent with its effects when administered prior to trigeminal ganglion stimulation. 6. In the anaesthetized dog, CP-122,288 and sumatriptan, at 1-300 micrograms kg-1, i.v., produced a dose-dependent reduction in carotid arterial blood flow and coronary arterial diameter. These data demonstrate that sumatriptan inhibits neurogenic inflammation in the rat (MED, 100 micrograms kg-1, i.v.), and produces vasoconstriction in the dog, over a similar dose-range. Interestingly, doses of CP-122,288 that inhibit neurogenic inflammation in rat dura mater (0.3-300 ng kg-1) were demonstrated to be devoid of vasoconstrictor activity in either the carotid or coronary vascular beds of dog. 7. These data demonstrate that in the rat, CP-122,288 is a highly potent and selective inhibitor of neurogenic inflammation in intracranial tissues, at doses which are devoid of vasoconstrictor activity in dog. Potentially, CP-122,288 may be of use for the acute treatment of migraine, without the risk of cardiovascular side-effects.

Anesthesia↗
PubMed2005

Role of neurogenic inflammation in pancreatitis and pancreatic pain.

Pain arising from pancreatic diseases can become chronic and difficult to treat. There is a paucity of knowledge regarding the mechanisms that sensitize neural pathways that transmit noxious information from visceral organs. In this review, neurogenic inflammation is presented as a possible amplifier of the noxious signal from peripheral organs including the pancreas. The nerve pathways that transmit pancreatic pain are also reviewed as a conduit of the amplified signals. It is likely that components of these visceral pain pathways can also be sensitized after neurogenic inflammation.

Animals↗
PubMed2004

Facilitated neurogenic inflammation in unaffected limbs of patients with complex regional pain syndrome.

Pain, edema, increased skin temperature, reddening and trophic changes characterize complex regional pain syndrome (CRPS). Recently, we have been able to show facilitated neurogenic inflammation on the affected limb. In the current study unaffected limbs were examined after resolution of the CRPS symptoms to assess possible generalized changes predisposing to CRPS. In 12 patients and in 12 healthy volunteers dermal microdialysis in combination with electrical C-fiber stimulation was employed to induce neuropeptide release. Dialysate protein concentration and axon reflex vasodilation were measured. Neither in patients nor in controls did electrical stimulation lead to protein extravasation, while axon reflex vasodilation was significantly enhanced even on the patients' unaffected limbs (P < 0.05). Our results support the hypothesis that facilitated neurogenic inflammation is a predisposing factor for CRPS. The lack of protein extravasation indicates that an initiating trauma is necessary to induce neuropeptide up-regulation in primary afferents.

Adult↗
PubMed2001

Is there a correlation between spreading depression, neurogenic inflammation, and nociception that might cause migraine headache?

The time course of propagation of scotoma and blood flow changes during migraine aura parallels the phenomenon of cortical spreading depression (CSD). It was proposed that CSD generates a sterile neurogenic inflammation in the meninges, which may then lead to the activation or sensitization of nociceptors, thus generating headache. We performed rat experiments in which the effect of CSD on plasma extravasation in the dura mater and on neuronal activity in deep laminae of the trigeminal nucleus was assessed in vivo. CSD did not alter dural plasma extravasation measured by means of bovine serum albumin-coupled flourescein (n = 17 rats) compared to the CSD-free contralateral side. In an in vitro model, the application of KCl to the dura at concentrations extracellularly found during CSD did not alter the release of calcitonin gene-related peptide and prostaglandin E2 from the dura. In 33 rats, neither single CSDs nor a series of CSDs altered ongoing neuronal activity or mechanical and/or thermal sensitivity of the deeply located neurons to stimulation of their receptive fields in the dura mater. These results are at variance with data that showed increased c-Fos labeling in superficial laminae of the trigeminal nucleus following CSD. They do not suggest that CSD initiates migraine headache via neurogenic inflammation.

Animals↗