Excitatory and Inhibitory Effects of Vagus Stimulation on Gastric Motility in the Cat

1963 ◽  
Vol 57 (4) ◽  
pp. 309-316 ◽  
Author(s):  
J. Martinson ◽  
A. Muren
Keyword(s):  
Gastric Motility ◽  
Inhibitory Effects ◽  
Vagus Stimulation

A reevaluation of the effects of stimulation of the dorsal motor nucleus of the vagus on gastric motility in the rat

2007 ◽  
Vol 292 (1) ◽  
pp. R291-R307 ◽  
Author(s):  
Maureen T. Cruz ◽  
Erin C. Murphy ◽  
Niaz Sahibzada ◽  
Joseph G. Verbalis ◽  
Richard A. Gillis
Keyword(s):  
Gastric Motility ◽  
Intragastric Balloon ◽  
Motor Nucleus ◽  
Inhibitory Effects ◽  
Inhibitory Pathways ◽  
Dorsal Motor Nucleus ◽  
Bilateral Vagotomy ◽  
Oxide Synthase ◽  
Intravenous Atropine ◽  
Stimulation Of

Our primary purpose was to characterize vagal pathways controlling gastric motility by microinjecting l-glutamate into the dorsal motor nucleus of the vagus (DMV) in the rat. An intragastric balloon was used to monitor motility. In 39 out of 43 experiments, microinjection of l-glutamate into different areas of the DMV rostral to calamus scriptorius (CS) resulted in vagally mediated excitatory effects on motility. We observed little evidence for inhibitory effects, even with intravenous atropine or with activation of gastric muscle muscarinic receptors by intravenous bethanechol. Inhibition of nitric oxide synthase with Nω-nitro-l-arginine methyl ester (l-NAME) HCl did not augment DMV-evoked excitatory effects on gastric motility. Microinjection of l-glutamate into the DMV caudal to CS produced vagally mediated gastric inhibition that was resistant to l-NAME. l-Glutamate microinjected into the medial subnucleus of the tractus solitarius (mNTS) also produced vagally mediated inhibition of gastric motility. Motility responses evoked from the DMV were always blocked by ipsilateral vagotomy, while responses evoked from the mNTS required bilateral vagotomy to be blocked. Microinjection of oxytocin into the DMV inhibited gastric motility, but the effect was never blocked by ipsilateral vagotomy, suggesting that the effect may have been due to diffusion of oxytocin to the mNTS. Microinjection of substance P and N-methyl-d-aspartate into the DMV also produced inhibitory effects attributable to excitation of nearby mNTS neurons. Our results do not support previous studies indicating parallel vagal excitatory and inhibitory pathways originating in the DMV rostral to CS. Our results do support previous findings of vagal inhibitory pathways originating in the DMV caudal to CS.

Mechanisms by which endogenous glucocorticoid protects against indomethacin-induced gastric injury in rats

2002 ◽  
Vol 283 (5) ◽  
pp. G1082-G1089 ◽  
Author(s):  
Ludmila Filaretova ◽  
Akiko Tanaka ◽  
Tohru Miyazawa ◽  
Shinichi Kato ◽  
Koji Takeuchi
Keyword(s):  
Gastric Motility ◽  
Protective Action ◽  
Microvascular Permeability ◽  
Gastric Injury ◽  
Functional Disorders ◽  
Gastric Lesions ◽  
Inhibitory Effects ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Adrenalectomized Rats

We investigated the mechanisms underlying the protective action of glucocorticoids against indomethacin-induced gastric lesions. One-week adrenalectomized rats with or without corticosterone replacement (4 mg/kg sc) were administered indomethacin (25 mg/kg sc), and gastric secretion (acid, pepsin, and mucus), motility, microvascular permeability, and blood glucose levels were examined. Indomethacin caused gastric lesions in sham-operated rats, with an increase in gastric motility and microvascular permeability as well as a decrease in mucus secretion. Adrenalectomy significantly worsened the lesions and potentiated these functional disorders. Glucose levels were lowered by indomethacin in sham-operated rats, and this response was enhanced by adrenalectomy. The changes observed in adrenalectomized rats were prevented by supplementations of corticosterone at a dose mimicking the indomethacin-induced rise in corticosterone, whereas the protective effect of corticosterone was attenuated by RU-38486, a glucocorticoid receptor antagonist. We conclude that the gastroprotective action of endogenous glucocorticoids may be provided by their support of glucose homeostasis and inhibitory effects on enhanced gastric motility and microvascular permeability as well as maintaining the production of mucus.

Jejunal regulation of gastric motility patterns: effect of extrinsic neural continuity to stomach

1990 ◽  
Vol 258 (1) ◽  
pp. G32-G37 ◽  
Author(s):  
M. P. Spencer ◽  
M. G. Sarr ◽  
N. J. Soper ◽  
N. S. Hakim
Keyword(s):  
Small Intestine ◽  
Gastric Motility ◽  
Contractile Activity ◽  
Inhibitory Effects ◽  
Extrinsic Denervation ◽  
Recovery Stage ◽  
Neural Input ◽  
Vagal Innervation ◽  
Stage 1

This study was designed to determine the role of extrinsic gastric innervation in mediating the inhibitory effects of jejunal infusion of mixed nutrients on canine interdigestive gastric motility patterns. Four dogs underwent transection of all extrinsic and intrinsic neural continuity to the stomach except for careful preservation of vagal innervation (stage 1). Antral manometry catheters, antral electrodes, intestinal electrodes, and a jejunal infusion catheter were placed. After a 2-wk recovery, stage 1 studies of myoelectric and contractile activity of the stomach and small bowel during fasting were recorded on four occasions during infusion of isomolar solutions of either nonnutrient NaCl (150 mM) or mixed nutrients (50% Meritene solution) into the jejunum at 2.9 ml/min for 6 h. Identical studies (stage 2) were repeated after completion of extrinsic denervation of the stomach by supradiaphragmatic vagotomy. In stage 1 studies, jejunal nutrients (83 kcal/h) inhibited the characteristic interdigestive cyclic motility patterns in the stomach and duodenum for greater than or equal to 172 min during jejunal infusion of mixed nutrients. After completion of extrinsic denervation (stage 2), jejunal infusion of nutrients had the same effects with inhibition of cyclic motility patterns in the stomach and small intestine. We concluded that inhibition of interdigestive gastric motility patterns by jejunally infused nutrients is mediated by hormonal mechanisms and not by nonvagal or vagal extrinsic neural input to the stomach.

Dual effects of acupuncture on gastric motility in conscious rats

2003 ◽  
Vol 285 (4) ◽  
pp. R862-R872 ◽  
Author(s):  
Makoto Tatewaki ◽  
Mary Harris ◽  
Kenichiro Uemura ◽  
Tomio Ueno ◽  
Etsuo Hoshino ◽  
...  
Keyword(s):  
Gastric Motility ◽  
Type A ◽  
Peak Amplitude ◽  
Phase Iii ◽  
Type B ◽  
Inhibitory Effects ◽  
Complex Type ◽  
Motility Index ◽  
Conscious Rats ◽  
Strain Gauge Transducer

The effects of manual acupuncture on gastric motility were investigated in 35 conscious rats implanted with a strain gauge transducer. Twenty (57.1%) rats showed no cyclic groupings of strong contractions ( type A), whereas 15 (42.9%) rats showed the phase III-like contractions of the migrating motor complex ( type B) in the fasting gastric motility. Acupuncture at the stomach (ST)-36 (Zusanli), but not on the back [Weishu, bladder (BL)-21], increased the peak amplitude of contractions to 172.4 ± 25.6% of basal in the type A rats ( n = 20, P < 0.05). On the other hand, the motility index for 60 min after the acupuncture was not affected by the acupuncture in this group. On the contrary, acupuncture decreased the peak amplitude and motility index to 72.9 ± 14.0% and 73.6 ± 16.2% in the type B rats ( n = 15, P < 0.05), respectively. The stimulatory and inhibitory effects of acupuncture observed in each type were reproducible on the separate days. In 70% of type A rats, acupuncture induced strong phase III-like contractions lasting for over 3 h that were abolished by atropine, hexamethonium, atropine methyl bromide, and vagotomy. Naloxone significantly shortened the duration of the stimulatory effects from 3.52 ± 0.21 to 1.02 ± 0.15 h ( n = 3, P < 0.05). These results suggest that acupuncture at ST-36 induces dual effects, either stimulatory or inhibitory, on gastric motility. The stimulatory effects are mediated in part via vagal efferent and opioid pathways.

Effect of suckling on gastric motility in lactating rats

1991 ◽  
Vol 261 (1) ◽  
pp. R38-R43 ◽  
Author(s):  
D. L. Helmreich ◽  
E. Thiels ◽  
A. F. Sved ◽  
J. G. Verbalis ◽  
E. M. Stricker
Keyword(s):  
Gastric Emptying ◽  
Paraventricular Nucleus ◽  
Gastric Motility ◽  
Male Rats ◽  
Inhibitory Effects ◽  
Gastric Function ◽  
Systemic Injection ◽  
Pituitary Secretion ◽  
Oxytocinergic Neurons ◽  
The Brain

Recent reports indicate that in male rats dehydration, LiCl, and cholecystokinin (CCK) each stimulate pituitary oxytocin (OT) secretion and also decrease gastric emptying and motility. In contrast, the present experiments demonstrate that nipple attachment and sucking by pups, a well-known stimulus for neurohypophysial secretion of OT, did not decrease gastric motility in lactating rats. Moreover, systemic injection of naloxone, which is known to potentiate the inhibitory effects of LiCl and CCK on gastric motility in male rats, had no effect on gastric motility of lactating rats while nursing. These data indicate that pituitary OT secretion from magnocellular neurons is not invariably linked to decreased gastric motility in rats. As such, our results support previous findings that inhibition of gastric motility is not secondary to the pituitary secretion of OT but allow a possible role for parvocellular oxytocinergic neurons that project from the hypothalamic paraventricular nucleus to the brain stem in the control of gastric function.

Gastric motility and food intake in rats after lesions of hypothalamic paraventricular nucleus

1992 ◽  
Vol 263 (1) ◽  
pp. R39-R44 ◽  
Author(s):  
L. M. Flanagan ◽  
J. Dohanics ◽  
J. G. Verbalis ◽  
E. M. Stricker
Keyword(s):  
Food Intake ◽  
Brain Stem ◽  
Paraventricular Nucleus ◽  
Local Anesthetic ◽  
Gastric Motility ◽  
Systemic Administration ◽  
Hypothalamic Paraventricular Nucleus ◽  
Inhibitory Effects

Systemic administration of cholecystokinin (CCK) or LiCl inhibits gastric motility and food intake in rats. Brain stem-projecting oxytocin (OT) neurons in the hypothalamic paraventricular nucleus (PVN) have been proposed to mediate the inhibitory effects of CCK and LiCl on gastric motility and food intake. In the present studies, we found that basal gastric motility was elevated in rats 12-20 h after knife-cut lesions of the PVN; however, this effect disappeared 3 days later. Furthermore, CCK and LiCl inhibited gastric motility at 12-20 h, 3 days, and 3 wk after PVN lesions, although their effects were blunted. Injection of the local anesthetic lidocaine into the PVN had effects similar to acute PVN lesions. In rats with PVN lesions, the inhibitory effects of CCK and LiCl on food intake were indistinguishable from those in sham-lesioned rats. We conclude that the PVN tonically inhibits gastric motility and that it participates in, but is not essential for, the inhibitory effects of CCK and LiCl on gastric motility and food intake in rats.

Effects of anorexigenic treatments on gastric motility in rats

1989 ◽  
Vol 256 (4) ◽  
pp. R955-R961 ◽  
Author(s):  
L. M. Flanagan ◽  
J. G. Verbalis ◽  
E. M. Stricker
Keyword(s):  
Food Intake ◽  
Gastric Motility ◽  
Gastric Distension ◽  
Reduce Food Intake ◽  
Inhibitory Effects ◽  
Gastric Function ◽  
Inhibit Food Intake ◽  
A Site ◽  
Gastric Contractions ◽  
Afferent Vagus

In these experiments we examined the effects on gastric motility of cholecystokinin, LiCl, hypertonic NaCl solution, gastric distension, and intraduodenal glucose loads, five dissimilar treatments known to reduce food intake in rats. In addition, we investigated whether any observed effects were dependent on the afferent vagus nerve by pretreating subjects with the neurotoxin capsaicin. Each of the five treatments virtually eliminated the gastric contractions seen after rats had consumed a large meal of chow; these effects were rapid in onset and continued for up to 30 min. The inhibitory effects of cholecystokinin and gastric distension were eliminated by pretreatment with capsaicin, whereas the effects of the other treatments were attenuated only slightly or not at all. Because most of these treatments have been shown to stimulate pituitary oxytocin secretion in rats as well as to inhibit food intake and gastric motility, these results are consistent with the hypothesis that the hypothalamic paraventricular nucleus is a site at which information is integrated in the coordinated control of food intake, gastric function, and neuroendocrine secretion.

Sign in / Sign up

Export Citation Format

Share Document