Abdominal Vagus Research Articles

Influence of H. pylori infection on gastric motor and sensory function in asymptomatic volunteers.

The effect of H. pylori infection on gastric motility and sensation is unclear. Our hypothesis is that H. pylori infection increases gastric sensation and reduces gastric accommodation and emptying. In eight H. pylori-positive and eight H. pylori-negative asymptomatic subjects, infection was proven by antral histology or culture. We evaluated: (1) gastric emptying of solids, (2) proximal gastric compliance, (3) fasting and postprandial proximal gastric tone and phasic contractions, (4) gastric sensation during balloon inflations or ingestion of cold water, and (5) abdominal vagal function. H. pylori infection was associated with lower gastric accommodation (median 75% postprandial increase in barostat balloon volume compared to fasting) when compared to the accommodation in uninfected volunteers (median 211% change from fasting). One H. pylori-positive subject had an abnormal abdominal vagal function test and her gastric accommodation response was reduced. Other motor and sensory functions in the two groups were similar. In asymptomatic volunteers, H. pylori infection and gastritis result in reduced accommodation (diastolic dysfunction) but no change in overall sensation or motor functions of the stomach.

Inhibition of bradykinin-induced plasma extravasation produced by noxious cutaneous and visceral stimuli and its modulation by vagal activity.

Intrathecally applied nicotine reduces bradykinin-induced plasma extravasation (BK-induced PE) in the rat knee joint. This depression is mediated by the hypothalamo-pituitary-adrenal (HPA) axis and is enhanced by interruption of impulse traffic in afferents of the abdominal vagus nerve. Like intrathecal nicotine, electrical stimulation of unmyelinated cutaneous fibers also depresses BK-induced PE, which is also dependent on an intact HPA axis. In this study, we investigated whether the inhibitory effect of intrathecal nicotine can be mimicked by noxious stimulation of skin and of viscera. Furthermore we determined whether this depression is potentiated after subdiaphragmatic vagotomy. Stimulation of visceral afferents in the peritoneum, by intraperitoneal capsaicin injection, dose-dependently decreased BK-induced PE. The capsaicin dose-response function was shifted by 1.5-2 orders of magnitude to the left after vagotomy. Stimulation of visceral afferents in the urinary bladder by capsaicin also dose-dependently reduced BK-induced PE, which similarly was potentiated after vagotomy. Transcutaneous stimulation of unmyelinated nociceptive afferents from the plantar skin of the paw depressed BK-induced PE. This depression had a threshold of approximately 0.25 Hz and was maximal at a stimulation frequency of approximately 1 Hz. After subdiaphragmatic vagotomy, the stimulus response function shifted to the left and the inhibition was significantly larger than in control, in the range of 0.125-1 Hz stimulation. These results show that noxious stimulation of skin and viscera depressed BK-induced PE and that such depression was potentiated after subdiaphragmatic vagotomy in a manner similar to that of intrathecally applied nicotine. Based on these observations, we hypothesize that intrathecal nicotine depresses BK-induced PE by exciting spinal nociceptive neurons or the central projections of nociceptive primary afferent neurons.

Antiemetic effects of N-3389, a newly synthesized 5-HT 3 and 5-HT 4 receptor antagonist, in ferrets

The antiemetic activity of N-3389 ( endo-3,9-dimethyl-3,9-diazabicyclo[3,3,1]non-7-yl-1 H-indazole-3-carboxamide dihydrochloride), a new 5-HT 3 and 5-HT 4 receptor antagonist, against cisplatin-, cyclophosphamide- and copper sulfate-induced emesis was investigated using ferrets. We also examined the effects of these agents on abdominal afferent vagus nerve activity in anesthetized ferrets. Both intraperitoneal (0.1–1.0 mg/kg) and oral (0.1–1.0 mg/kg) administration of N-3389 produced dose-dependent antiemetic effects. The time-course of cisplatin (10 mg/kg, i.p.)-induced emesis in another group of ferrets paralleled the increase in abdominal afferent vagus nerve activity induced by cisplatin (10 mg/kg, i.p.) and was inhibited by pretreatment with N-3389 (1.0 mg/kg, i.v.). Furthermore, the cisplatin (10 mg/kg, i.p.)-induced increase in abdominal afferent vagus nerve activity was markedly reduced by an additional injection of N-3389 (0.1–1.0 mg/kg, i.v.) in a dose-dependent manner. The antiemetic effects exhibited by N-3389 are probably due to the inhibition of 5-HT 3 and 5-HT 4 receptors on the abdominal afferent vagus nerves.

Effects of area postrema lesion and abdominal vagotomy on interleukin-1 β-induced norepinephrine release in the hypothalamic paraventricular nucleus region in the rat

Peripherally administered interleukin-1 β (IL-1 β) has been shown to increase extracellular norepinephrine (NE) concentration in the paraventricular nucleus (PVN) of the hypothalamus. The present study was carried out using an in vivo microdialysis technique in conscious rats in order to examine the possible involvement of the area postrema (AP) and the abdominal vagal afferent nerves in this effect. Extracellular NE concentrations in the PVN region were measured by high performance liquid chromatography with electrochemical detection. In AP-lesioned or abdominal-vagotomized rats, the NE increase was significantly attenuated compared to that in sham-operated rats; this reduction was greater in abdominal-vagotomized rats than in AP-lesioned rats. The results suggest that the AP as well as the abdominal vagal afferent nerves is involved in intraperitoneal (i.p.) administered IL-1 β-induced NE release in the PVN region.

Vagal branches involved in inhibition of bradykinin-induced synovial plasma extravasation by intrathecal nicotine and noxious stimulation in the rat.

1. Stimulation of cutaneous and spinal visceral nociceptive afferents and intrathecal nicotine reduces bradykinin-induced plasma extravasation (BK-induced PE) in the knee joint of the rat. This depression is mediated by the hypothalamo-pituitary-adrenal (HPA) axis and is potentiated by subdiaphragmatic vagotomy. It is believed that activity in vagal afferents tonically inhibits ascending impulse transmission in the neuraxis projecting to the hypothalamus. Vagotomy, by removing such inhibition, allows greater depression of BK-induced PE. In this study we determined whether the vagal afferents which negatively regulate activities of the HPA axis are present in all branches of the abdominal vagus nerves or only in specific branches. 2. We measured the depression of BK-induced PE elicited by graded stimulation of spinal visceral afferents with intraperitoneal capsaicin and by intrathecal nicotine in vagus-intact rats and in rats in which specific vagal branches were selectively interrupted. (i) Interruption of the coeliac branches mimicked the effect of total subdiaphragmatic vagotomy in potentiating the depression of BK-induced PE generated by intrathecal nicotine and by stimulation of spinal visceral afferents. (ii) Interruption of the gastric and hepatic branches of the abdominal vagus nerves together or individually did not affect the depression of BK-induced PE generated by the two stimuli. 3. These results indicate that afferent activity in coeliac and accessory coeliac vagal branches is involved in the regulation of the nociceptive system-initiated depression of BK-induced PE. The afferent fibres in these vagal branches involved probably monitor physiological events in abdominal visceral organs.

Inhibition of bradykinin-induced synovial plasma extravasation produced by intrathecal nicotine is mediated by the hypothalamopituitary adrenal axis.

1. Bradykinin (BK)-induced plasma extravasation (PE) in the rat knee joint, which is dependent to a large extent on the sympathetic innervation of the synovium, is powerfully inhibited, dose dependently, by intrathecal administration of nicotine, especially after interruption of the impulse traffic in afferents of the abdominal vagus nerve. In this study we investigated in vagotomized animals possible efferent pathways that might mediate the inhibition produced by the intrathecally applied nicotine. We studied the role of the sympathetic supply to the knee joint, of the sympathoadrenal system, and of the hypothalamopituitary-adrenal (HPA) axis in the ability of intrathecal nicotine to inhibit BK-induced PE in the knee joint. The experimental interventions performed were as follows: recording activity in the lumbar sympathetic trunk; antagonizing the effect of epinephrine, released from the adrenal medulla; acute interruption of the lumbar sympathetic trunks; hypophysectomy; and blockade of the glucocorticoid receptors. We employed acutely vagotomized animals because in these animals nicotine-induced inhibition is enhanced. 2. We found that hypophysectomy or blockade of the glucocorticoid receptors markedly attenuated the inhibition of BK-induced PE produced by intrathecal nicotine. 3. Intrathecal nicotine did not affect activity in the sympathetic chain. 4. Acute interruption of the lumbar sympathetic chain, which leaves the sympathetic terminals in the synovium intact but abolishes activity in the sympathetic postganglionic neurons, did not change the inhibition of BK-induced PE produced by intrathecal nicotine. 5. Blockade of the beta 2 adrenoceptors in the knee joint, preventing in this way potential effects of epinephrine released by the adrenal medulla, did not affect the inhibition of BK-induced PE produced by intrathecal nicotine. 6. The results of the present experiments strongly support the hypothesis that the powerful suppression of BK-induced PE in the knee joint generated by intrathecal nicotine is mediated via the HPA axis and not via activity in sympathetic neurons innervating the knee joint or the adrenal medulla. Future studies are needed to determine in which functional contexts this pathway is active in the control of PE in the synovia and of other aspects of inflammation.

Involvement of the vagus nerve, substance P and cholecystokinin in the regulation of intestinal blood flow

Intestinal blood flow was recorded in anesthetized rats and cats using laser-Doppler flowmetry (LDF). This new technique provides continuous and accurate measurements of the intestinal blood flow, without affecting the blood circulation. Electrical stimulation (1 ms, 5–30 V, 5–50 Hz) applied either afferent or efferent vagal fibres elicited changes in the intestinal blood flow consisting mainly of increases. Similar results were obtained upon applying chemical stimulation to intestinal sensory endings using cholecystokinin (CCK) or substance P (SP; 10–20 μg/kg intravenously given). Bilateral vagotomy and atropine treatment markedly reduced or suppressed these vascular effects. In addition, experiments in which the activation of gastrointestinal afferents were activated by applying electrical stimulation to the abdominal vagal nerves yielded similar results. Finally, these effects were reduced after selectively severing vagal afferents. It is concluded that intestinal blood changes may be triggered by activation of the sensory endings from the digestive organs through the vagal nerves.

Inhibition of food intake in rats by the K + channel opener cromakalim

We studied the effect of the K + channel opener cromakalim, which exhibits antihypertensive properties, on food intake in rats. Intraperitoneally injected cromakalim induced a dose-dependent (0.1, 0.5, and 1.0 mg/kg body wt.) reduction in food intake, which was associated with an inhibition of gastric emptying. The anorectic effect was not influenced by subdiaphragmatic vagotomy. Cromakalim's anorectic effect did not appear to be due to a learned taste aversion. Therefore, an intact abdominal vagus is not a prerequisite for cromakalim's anorectic effect.

Vasopressin responses to corticotropin-releasing factor and hypertonicity after truncal vagotomy in dogs.

Infusion of corticotropin-releasing factor (CRF) augments the plasma vasopressin response to infusion of hypertonic saline in conscious dogs. Furthermore, afferent vagal nerve input from the abdomen is involved in the control of vasopressin release and may be altered by CRF. The purpose of the present study was to characterize the effect of CRF on the vasopressin response to hypertonic saline and to determine if it is mediated by afferent input carried from the abdominal vagus. Conscious male dogs (n = 5) underwent infusion of isotonic saline (vehicle), CRF (10 or 20 ng.kg-1.min-1), hypertonic saline (0.2 mmol.kg-1.min-1), or the combination of CRF and hypertonic saline. Hypertonic saline increased plasma sodium from 147 +/- 1 to 153 +/- 1 meq/1 and plasma vasopressin from 2.5 +/- 0.1 to 5.8 +/- 0.4 pg/ml. CRF infusion alone had no effect on plasma vasopressin. The addition of 10 or 20 ng.kg-1.min-1 CRF augmented the vasopressin response to hypertonic saline to 7.7 +/- 1.7 and 6.9 +/- 0.3 pg/ml, respectively. Truncal vagotomy did not attenuate the vasopressin response to hypertonic saline with or without CRF infusion. We conclude that CRF augments the vasopressin response to hypertonic saline and that this effect is not mediated via afferents from the abdominal vagus.

The controls of fat intake.

To present evidence on the control of the size of fatty meals in the context of the result of interactions of orosensory positive-feedback and postingestive negative-feedback mechanisms activated by fat stimuli in rodent models of feeding and of obesity. We examined the effects of orosensory stimuli and postingestive stimuli in Sprague-Dawley rats, and in the genetically obese Zucker (fa/fa) rat. We used the sham feeding rat preparation to isolate the orosensory stimulating and postingestive satiating properties of oils. The negative-feedback satiating properties of fats were elicited by intestinal infusions of fats. The Zucker rat is an animal model of obesity with abnormal control of meal size and increased intake of fats. Using this model we further examined the interaction of orosensory and postingestive stimuli in the control of meal size. The orosensory properties of fats are sufficient to drive sham feeding and are not dependent on the postabsorptive metabolic consequences of oils in normal and Zucker rats. The satiating action of fats must act at preabsorptive sites because reduction of intake occurs before absorption of fat. The satiating potency of fats is dependent upon their specific chemical conformation and is mediated by endogenous cholecystokinin and afferent fibers of the abdominal vagus. We have found that oils produce significantly more orosensory positive feedback in obese Zucker rats than in lean rats in experimental tests of preference. This is probably the major abnormal mechanism responsible for the increased preference for fats that is characteristic of obese rats because we have not identified any significant decrease in the postingestive satiating potency of fats in obese Zucker rats. Fat intake is controlled by both orosensory and postingestive stimuli in normal and genetically obese rodents. In the Zucker rat the investigation of this model of genetic obesity has produced data that is congruent with the preference for high fat foods in obese people and suggests further experiments directed toward a deeper understanding of the controls of fat intake and how they are disordered.

Control of gallbladder contractions by cholecystokinin through cholecystokinin-A receptors in the vagal pathway and gallbladder in the dog

The mechanism of CCK action on gallbladder contractions in the physiological condition is unclear. Gallbladder contractions were monitored by means of chronically implanted force transducers in conscious dogs. Postprandial gallbladder contractions were partially inhibited by atropine and hexamethonium, and completely inhibited by devazepide. In vitro contractile response of canine gallbladder muscle strips to CCK-8 was also studied. CCK-8-induced muscle strip contraction was atropine and tetrodotoxin resistant, but was completely eliminated by devazepide. The existence of CCK receptors in the vagal nerve and gallbladder was examined by means of autoradiography. Forty-eight hours after ligation of the abdominal vagus, CCK-8 binding sites were found to accumulate in the subdiaphragmatic vagal nerve immediately proximal to the ligature, and similar binding sites were also found in the gallbladder smooth muscle layer. These binding sites were displaced by the addition of 10 −7 mol/l unlabeled CCK-8 and devazepide, but L-365,260 had no effect. In conclusion, it is considerable that postprandial CCK-induced gallbladder contractions are controlled through CCK-A receptors both on the vagal nerve in stimulating endogenous release of acetylcholine and on the gallbladder directly to stimulate muscle contraction in the dog.

NO mediates gastric relaxation after brief vagal stimulation in anesthetized dogs

In vitro studies showed that relaxations induced after vagal stimulation of the guinea pig stomach are mediated via nitric oxide (NO). The role of NO in canine gastric relaxation in response to vagal stimulation has as yet not been studied. The present study examined the influence of NG-nitro-L-arginine (L-NNA) on gastric relaxations after vagal nerve stimulation in the anesthetized dog. In beagle dogs (n = 7), the ventral and dorsal abdominal vagal nerves were connected to a pair of platinum electrodes. Gastric tone was measured by means of a barostat. Changes in gastric motility were measured with force transducers sutured on the fundus and the antrum. The cervical vagi were sectioned, and dogs were given atropine (0.2 mg/kg i.v.) and guanethidine (5 mg/kg i.v.). Electrical stimulation of the vagal trunks (19 V, 1-ms duration, for 15 s every 2 min, 1-30 Hz) induced frequency-dependent increases in volume. On the fundus, frequency-dependent relaxations could be observed (maximal effect at 5 mmHg and at 10 Hz). During electrical stimulation, the spontaneous antral contractions were completely blocked. After cessation of the stimulus, "rebound" contractions could be observed. L-NNA (5 mg/kg i.v.) completely blocked the increases in gastric volume and the relaxations on the fundus. On the antrum, however, contractions were observed during the electrical stimulation. L-Arginine (250 mg/kg i.v.) gradually restored the relaxations on electrical stimulation. This study demonstrates that NO mediates short-lasting vagally induced gastric relaxations in the anesthetized dog.

The anti‐emetic effects of CP‐99,994 in the ferret and the dog: role of the NK1 receptor

1. The selective NK1 receptor antagonist, CP-99,994, produced dose-related (0.1-1.0 mg kg-1, s.c.) inhibition of vomiting and retching in ferrets challenged with central (loperamide and apomorphine), peripheral (CuSO4) and mixed central and peripheral (ipecac, cisplatin) emetic stimuli. 2. Parallel studies with the enantiomer, CP-100,263 (1 mg kg-1, s.c.), which is > 1,000 fold less potent as a NK1 antagonist, indicated that it was without significant effect against CuSO4, loperamide, cisplatin and apomorphine-induced emesis. Against ipecac, it inhibited both retching and vomiting, expressing approximately 1/10th the potency of CP-99,994. 3. The 5-HT3 receptor antagonist, tropisetron (1 mg kg-1, s.c.) inhibited retching and vomiting to cisplatin and ipecac, but not CuSO4 or loperamide. 4. CP-99,994 (1 mg kg-1, i.v.) blocked retching induced by electrical stimulation of the ventral abdominal vagus without affecting the cardiovascular response, the apnoeic response to central vagal stimulation or the guarding and hypertensive response to stimulation of the greater splanchnic nerves. CP-99,994 (1 mg kg-1, i.v.) did not alter baseline cardiovascular and respiratory parameters and it failed to block the characteristic heart rate, blood pressure and respiratory rate/depth changes in response to i.v. 2-methyl-5-HT challenge (von Bezold-Jarisch reflex). 5. Using in vitro autoradiography, [3H]-substance P was shown to bind to several regions of the ferret brainstem with the density of binding in the nucleus tractus solitarius being much greater than in the area postrema. This binding was displaced by CP-99,994 in a concentration-related manner. 6. In dogs, CP-99,994 (40 micrograms kg-1 bolus and 300 micrograms kg-1 h-1, i.v.) produced statistically significant reductions in vomiting to CuSO4 and apomorphine as well as retching to CuSO4. 7. Together, these studies support the hypothesis that the NK1 receptor antagonist properties of CP-99,994 are responsible for its broad spectrum anti-emetic effects. They also suggest that CP-99,994 acts within the brainstem, most probably within the nucleus tractus solitarius although the involvement of the area postrema could not be excluded.

Abdominal vagal stimulation excites bulbospinal barosensitive neurons in the rostral ventrolateral medulla

We used extracellular recordings to examine the central pathway whereby electrical stimulation of abdominal vagal afferents elevates arterial pressure in the rabbit. Bulbospinal neurons in the rostral ventrolateral medulla were identified by antidromic activation from the dorsolateral funiculus of the thoracic spinal cord. Their barosensitivity was assessed by their response to intravenous phenylephrine and by their cardiac cycle-related rhythmicity. We used peristimulus histogram procedures to assess the effect of electrical stimulation of abdominal vagal afferents on the discharge rate of these neurons. Electrical stimulation (one to three pulses) activated 98 of 123 neurons tested (80%), had no effect on 22 neurons (18%) and inhibited the remaining three neurons. Latency to peak excitation was 228 +/- 3 ms, indicating that the conduction velocity of the vagal afferents was about 0.6 m/s, in the unmyelinated fibre range. Lower oesophageal distension with a balloon excited 22 of 48 neurons (46%), inhibited 12 neurons (25%) and had no effect on the remaining 14 cells (29%). Vagally induced excitation was reduced by aortic depressor nerve stimulation in nine of 13 neurons. Lightly touching the animal's back and legs had no effect on 56 of 60 neurons. Nociceptive stimuli failed to affect 47 of 60 neurons tested. No excitation was seen with electrical stimulation of the sciatic or central ear nerves. Our study identifies a robust excitatory input from the abdominal vagus to bulbospinal barosensitive neurons in the rostral ventrolateral medulla. Relevant physiological stimuli include lower oesophageal distension. The pathways may be relevant to cardiovascular changes which accompany upper gastrointestinal function.

Abdominal vagotomy attenuates the inhibiting effect of mannitol on the ingestive behavior of rats.

Intact and abdominally vagotomized rats were offered for ingestion during a 30-min period a saccharin and glucose solution or another with 0.1 M mannitol added. The addition of mannitol to the test solution caused a large reduction in intake of intact rats caused by a very rapid decline in the rate of licking during the test. This did not occur with the vagotomized rats. This demonstrates that abdominal vagal nerves are necessary for the inhibitory effect of mannitol on the ingestive behavior of rats. Vagotomized rats also differed from the intact ones by ingesting less of the mannitol-free solution. This was suggested to result from accelerated gastric clearance, leading to abnormally rapid stimulation of negative feedback from the small intestine conveyed to the CNS by extravagal pathways.

Cholecystokinin changes the duration but not the rate of licking in vagotomized rats.

Abdominal vagotomy markedly reduces or abolishes the inhibitory effect of cholecystokinin (CCK-8) on meal size. To investigate the rate and microstructure of licking underlying this phenomenon, licking was measured throughout a meal of milk in intact and vagotomized rats after intraperitoneal injections of isotonic saline or CCK-8. CCK-8 increased the slope of the decay of licking, decreased the efficiency of licking, and decreased the duration of licking in intact rats but had no effect on either the slope of the decay of licking or the efficiency of licking, but it increased the duration of licking in vagotomized rats. These results demonstrate that abdominal vagal nerves are necessary for CCK-8 to increase the rate of decay of licking, but nonvagal mechanisms mediate the effect of CCK-8 on duration of licking.

Abdominal vagal inputs to catecholamine neurons in the ventrolateral medulla.

Stimulation of the abdominal vagus nerve increases arterial pressure and causes secretion of vasopressin. We have shown in rabbits that the arterial pressure increases are mediated by activation of barosensitive bulbospinal neurons in the C1 region of the rostral medulla. Secretion of vasopressin involves activation of neurons in the A1 region of the caudal ventrolateral medulla. Neuroanatomical studies with Fos indicate that approximately 50% of the C1 area cells are C1 neurons. Approximately 70% of the A1 area cells are A1 neurons. These neurons may mediate physiological responses occurring during abdominal malaise resulting from ingestion of toxins. Our discovery of a major excitatory input to A1 and C1 neurons from the abdominal vagus should prove useful in studies of the function of these neurons.

Vagal afferent innervation of rat abdominal paraganglia as revealed by anterograde DiI-tracing and confocal microscopy.

Abdominal vagal afferent fibers were selectively labeled by injecting the fluorescent carbocyanine dye DiI into the left nodose ganglion of rats. Almost all paraganglia that were distributed along the five major abdominal vagal branches and their subbranches were found to be innervated by labeled vagal afferents. Laser scanning confocal microscopy with its single optical sectioning and three-dimensional reconstruction capabilities were used to analyze this innervation in more detail for paraganglia near the vagal hepatic branch and liver hilus. Furthermore, in double-labeling studies, it was demonstrated that a large percentage of the vagally innervated glomus cells were capable of catecholamine synthesis on the basis of their positive staining for tyrosine hydroxylase antibody. These findings support the concept of a chemoreceptive function for the abdominal paraganglia.

Subdiaphragmatic vagotomy does not influence the anorectic effect of amylin.

Amylin injected IP reduced food intake for 2-4 h in subdiaphragmatically vagotomized and in sham-vagotomized rats. The magnitude of the anorectic effect of 0.5 microgram/kg amylin was similar to that of 2.5 micrograms/kg amylin but the duration of the effect was somewhat shorter with the low dose. Amylin (1 microgram/kg, IP) had no influence on gastric emptying. In conclusion, the hypophagic effect of peripherally administered amylin does not depend on an intact abdominal vagus or on an indirect effect via gastric emptying. It may therefore be hypothesized that amylin has a central site of action.

Organization of vestibular inputs to nucleus tractus solitarius and adjacent structures in cat brain stem.

The vestibular system is involved in maintaining stable blood pressure and respiration during changes in posture and is essential for eliciting motion sickness-related vomiting. Because the nucleus tractus solitarius (NTS) participates in the regulation of sympathetic and inspiratory outflow and the triggering of emesis, we tested the hypothesis that this region receives vestibular inputs in cats. In one set of experiments, microinjections of the tracer Phaseolus vulgaris leucoagglutinin into the medial and inferior vestibular nuclei labeled projections to the middle and lateral regions of the NTS. In electrophysiological experiments, electrical stimulation of the vestibular nerve modified the firing rates of neurons located in the same regions. Some neurons with vestibular inputs received convergent signals from the abdominal vagus nerve and could potentially mediate motion sickness-related vomiting. Others received convergent baroreceptor inputs and could act as a substrate for some components of vestibulosympathetic reflexes. In contrast, inspiratory neurons in the dorsal respiratory group received little vestibular input, suggesting that vestibulorespiratory reflexes are mediated by cells located elsewhere.