Axon Reflex and Neurogenic Inflammation in Vagal Afferent Nerves

2005 ◽  
pp. 431-464 ◽  
Author(s):  
Giovanni Piedimonte
Keyword(s):  
Neurogenic Inflammation ◽  
Axon Reflex ◽  
Afferent Nerves ◽  
Vagal Afferent

Neurogenic inflammation: Axon reflex in pigs

1989 ◽  
Vol 26 (1-2) ◽  
pp. 231-232 ◽  
Author(s):  
Fr. -K. Pierau ◽  
J. Szolcsányi
Keyword(s):  
Neurogenic Inflammation ◽  
Axon Reflex

scholarly journals Subdiaphragmatic vagal afferent nerves modulate visceral pain

2008 ◽  
Vol 294 (6) ◽  
pp. G1441-G1449 ◽  
Author(s):  
S. L. Chen ◽  
X. Y. Wu ◽  
Z. J. Cao ◽  
J. Fan ◽  
M. Wang ◽  
...  
Keyword(s):  
Vagus Nerve ◽  
High Intensity ◽  
Visceral Pain ◽  
Light Level ◽  
Vagal Afferents ◽  
Abdominal Muscles ◽  
Low Intensity ◽  
C Fibers ◽  
Afferent Nerves ◽  
Vagal Afferent

Activation of the vagal afferents by noxious gastrointestinal stimuli suggests that vagal afferents may play a complex role in visceral pain processes. The contribution of the vagus nerve to visceral pain remains unresolved. Previous studies reported that patients following chronic vagotomy have lower pain thresholds. The patient with irritable bowel syndrome has been shown alteration of vagal function. We hypothesize that vagal afferent nerves modulate visceral pain. Visceromotor responses (VMR) to graded colorectal distension (CRD) were recorded from the abdominal muscles in conscious rats. Chronic subdiaphragmatic vagus nerve sections induced 470, 106, 51, and 54% increases in VMR to CRD at 20, 40, 60 and 80 mmHg, respectively. Similarly, at light level of anesthesia, topical application of lidocaine to the subdiaphragmatic vagus nerve in rats increased VMR to CRD. Vagal afferent neuronal responses to low or high-intensity electrical vagal stimulation (EVS) of vagal afferent Aδ or C fibers were distinguished by calculating their conduction velocity. Low-intensity EVS of Aδ fibers (40 μA, 20 Hz, 0.5 ms for 30 s) reduced VMR to CRD at 40, 60, and 80 mmHg by 41, 52, and 58%, respectively. In contrast, high-intensity EVS of C fibers (400 μA, 1 Hz, 0.5 ms for 30 s) had no effect on VMR to CRD. In conclusion, we demonstrated that vagal afferent nerves modulate visceral pain. Low-intensity EVS that activates vagal afferent Aδ fibers reduced visceral pain. Thus EVS may potentially have a role in the treatment of chronic visceral pain.

Mechanistic studies of acid-evoked coughing in anesthetized guinea pigs

2006 ◽  
Vol 291 (2) ◽  
pp. R454-R463 ◽  
Author(s):  
Brendan J. Canning ◽  
David G. Farmer ◽  
Nanako Mori
Keyword(s):  
Citric Acid ◽  
Guinea Pigs ◽  
Transient Receptor Potential ◽  
Superior Laryngeal Nerve ◽  
Transient Receptor Potential Vanilloid ◽  
Receptor Antagonists ◽  
Tracheal Mucosa ◽  
C Fibers ◽  
Afferent Nerves ◽  
Vagal Afferent

Experiments carried out in conscious guinea pigs suggest that citric acid-evoked coughing is partly mediated by transient receptor potential vanilloid type 1 (TRPV1) receptor-dependent activation of tachykinin-containing, capsaicin-sensitive C fibers. In vitro electrophysiological analyses indicate, however, that acid also activates capsaicin-sensitive and -insensitive vagal afferent nerves by a TRPV1-independent mechanism, and studies in anesthetized guinea pigs show that coughing evoked by acid is mediated by activation of capsaicin-insensitive vagal afferent nerves. In the present study, we have characterized the mechanisms of citric acid-evoked coughing in anesthetized guinea pigs. Drugs were administered directly to the Krebs buffer perfusing the extrathoracic trachea. Citric acid was applied topically to the tracheal mucosa, directly into the tracheal perfusate in increasing concentrations and at 1-min intervals. Citric acid dose dependently evoked coughing in anesthetized guinea pigs. This was mimicked by hydrochloric acid but not by sodium citrate. The coughing evoked by acid was nearly or completely abolished by TTX or by cutting the recurrent laryngeal nerves. Perfusing the trachea with a low Cl− buffer potentiated the acid-induced cough reflex. In contrast, prior capsaicin desensitization, 10 μM capsazepine, Ca2+-free perfusate, 0.1 μM iberiotoxin, 1 μM atropine, 10 μM isoproterenol, 10 μM albuterol, 3 μM indomethacin, 0.1 μM HOE-140, a combination of neurokinin1 (NK1; CP-99994), NK2 (SR-48968), and NK3 (SB-223412) receptor antagonists (0.1 μM each), a combination of histamine H1 (3 μM pyrilamine) and cysLT1 (1 μM ICI-198615) receptor antagonists, superior laryngeal nerve transection, or epithelium removal did not inhibit citric acid-evoked coughing. These and other data indicate that citric acid-evoked coughing in anesthetized guinea pigs is mediated by direct activation of capsaicin-insensitive vagal afferent nerves, perhaps through sequential activation of acid-sensing ion channels and chloride channels.

scholarly journals Gentle Manual Acupuncture Could Better Regulate Gastric Motility and Vagal Afferent Nerve Discharge of Rats with Gastric Hypomotility

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Yangyang Liu ◽  
Yang Bai ◽  
Yue Pan ◽  
Zhifang Xu ◽  
Yuxin Fang ◽  
...  
Keyword(s):  
Gastric Motility ◽  
Underlying Mechanism ◽  
Afferent Nerve ◽  
Manual Acupuncture ◽  
Intensity Effect ◽  
Afferent Nerves ◽  
Strong Stimulation ◽  
Vagal Afferent ◽  
Acupuncture Effects ◽  
Nerve Discharge

The variation of stimulus intensity of manual acupuncture (MA) may produce diverse acupuncture effects. However, the intensity-effect relationship and the underlying mechanism of MA are still elusive. In this study, the effects of MA regulation of gastric motility were investigated after lifting-thrusting MA treatment with four different frequencies (1 Hz, 2 Hz, 3 Hz, and 4 Hz) at ST36. The experiments were conducted on rats with gastric hypomotility caused by atropine. The results showed that the gastric motility amplitude decreased after atropine injection, while the treatment of four types of MA affected the gastric motility amplitude in varying degrees. Specifically, 2 Hz MA exhibited the most effective results, while 4 Hz MA had the least effect; the effects of 1 Hz MA and 3 Hz MA were between the effects induced with 2 Hz and 4 Hz. Furthermore, the response of gastric vagal afferent nerve discharge and gastric motility was examined after MA treatment with frequencies of 2 Hz and 4 Hz, respectively, on ST36 in order to elucidate the mechanism of MA regulation of gastric motility. The results showed that 2 Hz MA was able to increase the amplitude of gastric motility and discharge frequency of gastric vagal afferent nerves, while 4 Hz MA exhibited seldom effects. These findings suggest that gentle MA (2 Hz) has more stimulating effects than strong stimulation with MA (4 Hz) on gastric hypomotility. In addition, gastric motility regulated by MA was associated with vagal afferent nerve activation.

Early vasodilator response to anodal current application in human is not impaired by cyclooxygenase-2 blockade

2005 ◽  
Vol 288 (4) ◽  
pp. H1668-H1673 ◽  
Author(s):  
Maylis Tartas ◽  
Philippe Bouyé ◽  
Audrey Koïtka ◽  
Sylvain Durand ◽  
Yves Gallois ◽  
...  
Keyword(s):  
Neurogenic Inflammation ◽  
Current Application ◽  
Primary Afferent ◽  
Axon Reflex ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilatation ◽  
Afferent Fibers ◽  
Primary Afferent Fibers ◽  
Cox 2 ◽  
Cox 1

It is generally acknowledged that cutaneous vasodilatation in response to monopolar galvanic current application would result from an axon reflex in primary afferent fibers and the neurogenic inflammation resulting from neuropeptide release. Previous studies suggested participation of prostaglandin (PG) in anodal current-induced cutaneous vasodilatation. Thus the inducible cyclooxygenase (COX) isoform (COX-2), assumed to play a key role in inflammation, should be involved in the synthesis of the PG that is released. Skin blood flow (SkBF) variations induced by 5 min of 0.1-mA monopolar anodal current application were evaluated with laser-Doppler flowmetry on the forearm of healthy volunteers treated with indomethacin (COX-1 and COX-2 inhibitor), celecoxib (COX-2 inhibitor), or placebo. SkBF was indexed as cutaneous vascular conductance (CVC), expressed as percentage of heat-induced maximal CVC (%MVC). Urinalyses were performed to test celecoxib treatment efficiency. No difference was found in CVC values at rest: 14.3 ± 4.0, 11.9 ± 3.2, and 10.9 ± 2.0% MVC after indomethacin, celecoxib, and placebo treatment, respectively. At 10 min after the onset of anodal current application, CVC values were 22.2 ± 4.9% MVC (not significantly different from rest) with indomethacin, 85.7 ± 15.3% MVC ( P < 0.001 vs. rest) with celecoxib, and 70.4 ± 13.1% MVC ( P < 0.001 vs. rest) with placebo. Celecoxib significantly depressed the urinary prostacyclin metabolite 6-keto-PGF1α ( P < 0.05 vs. placebo). Indomethacin, but not celecoxib, significantly inhibited the anodal current-induced vasodilatation. Thus, although they are assumed to result from an axon reflex in primary afferent fibers and neurogenic inflammation, these results suggest that the early anodal current-induced vasodilatation is mainly dependent on COX-1-induced PG synthesis.

Inhibitory effects on intake of cholecystokinin-8 and cholecystokinin-33 in rats with hepatic proper or common hepatic branch vagal innervation

2005 ◽  
Vol 289 (2) ◽  
pp. R456-R462 ◽  
Author(s):  
S. Eisen ◽  
R. J. Phillips ◽  
N. Geary ◽  
E. A. Baronowsky ◽  
T. L. Powley ◽  
...  
Keyword(s):  
Intraperitoneal Administration ◽  
Inhibitory Effect ◽  
Inhibitory Interaction ◽  
Afferent Nerves ◽  
Afferent Fibers ◽  
Vagal Nerves ◽  
Vagal Innervation ◽  
Afferent Vagal ◽  
Vagal Afferent ◽  
Hepatic Branch

The relative potencies of cholecystokinin (CCK)-8 and CCK-33 for decreasing meal size depend on the route of administration. Inhibitory potencies are equal after intraperitoneal administration, but CCK-33 is significantly more potent after intraportal administration. This suggests that CCK-33 is a more effective stimulant of hepatic afferent vagal nerves than is CCK-8. To investigate this possibility, we administered both peptides intraperitoneally in rats with abdominal vagotomies that spared only the hepatic proper vagal nerves (H) and in rats with abdominal vagotomies that spared the common hepatic branch that contains the fibers of the hepatic proper and gastroduodenal nerves (HGD). The vagal afferent innervation in H and HGD rats was verified with a wheat germ agglutinin-horseradish tracer strategy. Intraperitoneal administration of CCK-33 decreased 30-min intake of 10% sucrose in H rats as much as in sham rats, but CCK-8 decreased intake significantly less in H rats than in sham rats. The larger inhibitory effect of CCK-33 than of CCK-8 in H rats is consistent with the hypothesis that CCK-33 is a more effective stimulant of the hepatic proper vagal afferent nerves than CCK-8. In contrast to the results in H rats, the inhibitory potencies of both peptides were significantly and equivalently reduced in HGD rats compared with sham rats. This suggests that there is an inhibitory interaction between the stimulation of the gastroduodenal and hepatic proper afferent fibers by CCK-33.

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