Activity of respiratory-related oropharyngeal and laryngeal motoneurones during fictive vomiting in the decerebrate cat

doi:10.1016/0006-8993(90)91094-W

Brain Research

Volume 513, Issue 1, 9 April 1990, Pages 101-105

https://doi.org/10.1016/0006-8993(90)91094-W Get rights and content

Abstract

Activities of respiratory laryngeal and oropharyngeal respiratory nerves were studied during fictive vomiting elicited by supradiaphragmatic vagus nerve stimulation in the decerebrate cat. Inspiratory laryngeal nerves were strongly inhibited throughout the retching and expulsion phase. Glossopharyngeal, hypoglossal and expiratory laryngeal nerves were coactivated with the phrenic and abdominal nerve bursts. The pharyngeal branch of the vagus nerve discharged during the phrenic and abdominal inter-burst of the retching phase, and was silent during the abdominal expulsion. These activities permit speculation about the role of upper airway muscles during vomiting.

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Electrical and chemical stimulation of the nucleus raphe magnus inhibits induction of retching by afferent vagal fibers
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Like pain sensation, vomiting is induced by C afferent fibers of the vagus nerve. Therefore, it can be assumed to be suppressed by the descending inhibitory system (DIS) of pain. In this study we examined this possibility in immobilized decerebrated dogs. Fictive retching was induced by the stimulation of abdominal afferent vagal fibers (stim-abdVAs) and identified by activity patterns of efferent discharges of the phrenic and abdominal muscle nerves. The induction of retching was suppressed by weak stimulation (20 μA, 20 Hz, 0.5 ms duration) of the pontine area corresponding to the nucleus raphe magnus (NRM). Stronger suppressions were produced by stimulation of the rostral part of the NRM at the pontine level where the abducen nucleus exists. Pontamine sky blue, an excitatory neurotoxin, which was microinjected into the NRM area in 5 dogs, completely suppressed the induction of retching during the injection period. The NRM area at the level of the abducen nucleus was commonly stained by the dye in the 5 dogs. These results suggest that the DIS of pain suppresses the induction of retching by afferent vagal fibers.
The site of the anti-emetic action of tachykinin NK<inf>1</inf> receptor antagonists may exist in the medullary area adjacent to the semicompact part of the nucleus ambiguus
1999, Brain Research
NK₁ receptor antagonists have been shown to act centrally and to produce a broad-spectrum anti-emetic action. To determine precisely the site of this action, we microinjected GR205171, an NK₁ receptor antagonist, into the left medulla oblongata in decerebrate paralyzed dogs. The right medulla was transected 2.5 mm rostral to the obex to eliminate the emetic function of that half. Fictive retching induced by vagal stimulation was still observed after each of 32 injections (0.5–5 μg in 1–30 μl) in the area ventrolateral to the solitary complex in six dogs. Retching was also observed for 30 min or more after all but 2 of 30 injections (0.5–1 μg in 0.5–1 μl) in the area dorsal to the retrofacial nucleus in 17 dogs. In contrast, retching disappeared within 5–30 min after each of 20 injections (0.5–1 μg in 1 μl) in the area adjacent to the semicompact part of the nucleus ambiguus (scAMB) in 15 dogs. The threshold dose for abolition of the retching response was examined in seven dogs and was about 0.1 ng in 1 μl. The maximum velocity of salivation occurred before the onset of retching and significantly decreased after its abolition. These results suggest that the site of the anti-emetic action of NK₁ receptor antagonists may lie in a limited area adjacent to the scAMB, and that neurons in the site induce prodromal signs and retching in a sequential manner.
The tachykinin NK<inf>1</inf> receptor antagonist GR205171 abolishes the retching activity of neurons comprising the central pattern generator for vomiting in dogs
1999, Neuroscience Research
Tachykinin NK₁ receptor antagonists are known to act centrally and to have broad-spectrum antiemetic effects, but their precise site of action has not yet been defined. To identify this site, the effects of the NK₁ receptor antagonist GR205171 on the activities of neurons comprising the central pattern generator (CPG) for vomiting were observed in decerebrate paralyzed dogs. A non-respiratory neuron in each of nine dogs was considered to be a CPG neuron based on its response to abdominal vagal stimulation, its location in the CPG area in the reticular formation dorsomedial to the retrofacial nucleus, its firing patterns in prodromal and retching phases and its response to apomorphine. In response to vagal stimulation at 3–10 Hz, the firing of these neurons transiently increased at the onset of stimulation (fast component), gradually increased again (slow component), and finally developed into rhythmic bursts synchronous with retching bursts of the phrenic and abdominal muscle nerves. GR205171 (25–50 μg/kg, i.v.) abolished the slow component and retching bursts in the neurons, and the retching activities of both nerves, but did not change the fast component. The responses of these neurons to repetitive pulse–train vagal stimulation exhibited a vigorous ‘wind-up’ and finally developed into retching bursts. Both the ‘wind-up’ phenomenon and retching bursts disappeared after the application of GR205171. These results suggest that the site of the antiemetic action of NK₁ receptor antagonists is located in the CPG or in the pathway connecting the solitary nucleus to the CPG.
The tachykinin NK<inf>1</inf> receptor antagonist GR205171 prevents vagal stimulation-induced retching but not neuronal transmission from emetic vagal afferents to solitary nucleus neurons in dogs
1998, Brain Research
Tachykinin NK₁ receptor antagonists injected into the medulla oblongata are known to abolish vomiting induced by vagal afferent stimulation. Emetic vagal afferents have been shown to synapse with neurons in the medial solitary nucleus (mNTS), which suggests that substance P is a transmitter in the synapse. To examine this possibility, the effects of GR205171, an NK₁ receptor antagonist, on retching and mNTS neuronal responses to the stimulation of abdominal vagal afferents were investigated in decerebrate dogs. GR205171 (0.05–0.7 mg kg⁻¹, i.v.) abolished retching induced by either vagal or mNTS stimulation within 5 min. Firing of mNTS neurons in response to pulse-train and sustained vagal stimulation did not change even after the abolition of retching. Similarly, GR205171 did not have any effects on mNTS evoked potentials induced by pulse-train vagal stimulation. In about 20% of mNTS neurons, the peak firing frequency was facilitated to about 150% with repetitive pulse-train vagal stimulation. This facilitation remained even after the abolition of retching. Administration of GR205171 (1 mg ml⁻¹, 30 μl) into the 4th ventricle abolished retching, with latencies in excess of 120 min. These results suggest that substance P does not participate in synaptic transmission between emetic vagal afferents and mNTS neurons in dogs.
Upper airway motor outputs during vomiting versus swallowing in the decerebrate cat
1998, Brain Research
Swallowing and vomiting are antagonistic motor acts; nevertheless, vomiting can be immediately followed by swallowing. The purpose of this study was to clarify the interrelationship between these two behaviors, particularly in regard to comparing the upper airway motor patterns at the end of the expulsion phase with those during subsequent swallowing. Experiments were conducted using both paralyzed and non-paralyzed decerebrate cats, in which recordings were obtained either from upper airway muscles, the diaphragm and abdominal muscles or from the nerves that innervate those muscles. The activity patterns of most nerves recorded in paralyzed animals were consistent with the behavior recorded in non-paralyzed animals from the muscles innervated by those nerves, with the exception of the cricothyroid and stylopharyngeus muscles. Vomiting can be divided into a series of retches followed by expulsion, which itself can be further subdivided into three phases. The final stage of expulsion, characterized by burst-like exaggerated activity of the laryngeal elevator thyrohyoid and the pharyngeal constrictors, proved to be different from pharyngeal swallowing, as judged from differences in the spatio-temporal patterns of the upper airway motor outputs. However, post-vomiting swallowing activity was still observed even after total deafferentation of the laryngeal and pharyngeal areas in paralyzed animals. It is therefore likely that the central processes for vomiting and swallowing closely relate in generating these two behaviors.
Capsaicin in the 4th ventricle abolishes retching and transmission of emetic vagal afferents to solitary nucleus neurons
1997, European Journal of Pharmacology
Systemic tachykinin NK1 receptor antagonists and resiniferatoxin are known to abolish vomiting mediated by vagal afferents. Emetic vagal afferents have been shown to make synaptic contact with neurons in the medial solitary nucleus. These results suggest that substance P participates in the synapse as a mediator. To examine this possibility, the effects of 4th-ventricular application of capsaicin (0.033–33 mM, 20–30 μl) and resiniferatoxin (1.6–160 μM, 20–30 μl) on the activity of neurons in the medial solitary nucleus and fictive retching induced by vagal stimulation were observed in paralyzed decerebrate dogs. Capsaicin (33 mM) and resiniferatoxin (160 μM) initially increased the neuronal firing and occasionally produced retching, then abolished both neuronal and retching responses. However, stimulation of the medial solitary nucleus continued to provoke retching. Field potential changes in the medial solitary nucleus evoked by pulse-train vagal stimulation decreased in amplitude, but did not disappear. Latencies of neuronal firing and evoked potentials were about 300 ms. These results suggest that emetic vagal afferents are capsaicin-sensitive C fibers which may have substance P as an excitatory transmitter or modulator.

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Activity of respiratory-related oropharyngeal and laryngeal motoneurones during fictive vomiting in the decerebrate cat

Abstract

Neurosci. Lett.

Br. J. Anaesthesiol.

Exp. Neurol.

Pharmacol. Methods

Brain Research

Brain Research

Localisation et étude des neurones respiratoires bulbaires. Mise en jeu antidromique par stimulation spinale ou vagale

J. Physiol. (Paris)

L'activité spontanée du sphincter oesophagien supérieur chez le mouton. Ses variations au cours de la déglutition et de la rumination

J. Physiol. (Paris)

Pharyngeal motoneurones: respiratory-related activity and responses to laryngeal afferents in the decerebrate cat

Exp. Brain Res.

Studies on vomiting

J. Pharmacol. Exp. Ther.