scholarly journals Noradrenergic neurons in the rat solitary nucleus participate in the esophageal-gastric relaxation reflex

2003 ◽  
Vol 285 (2) ◽  
pp. R479-R489 ◽  
Author(s):  
R. C. Rogers ◽  
R. A. Travagli ◽  
G. E. Hermann
Keyword(s):  
Large Population ◽  
Central Nucleus ◽  
Motor Nucleus ◽  
Adrenoceptor Antagonist ◽  
Dorsal Motor Nucleus ◽  
Efferent Neurons ◽  
Nos Inhibitor ◽  
Immunohistochemical Techniques ◽  
Oxide Synthase ◽  
Local Brain

Activation of esophageal mechanosensors excites neurons in and near the central nucleus of the solitary tract (NSTc). In turn, NSTc neurons coordinate the relaxation of the stomach [i.e., the receptive relaxation reflex (RRR)] by modulating the output of vagal efferent neurons of the dorsal motor nucleus of the vagus (DMN). The NSTc area contains neurons with diverse neurochemical phenotypes, including a large population of catecholaminergic and nitrergic neurons. The aim of the present study was to determine whether either one of these prominent neuronal phenotypes was involved in the RRR. Immunohistochemical techniques revealed that repetitive esophageal distension caused 53% of tyrosine hydroxylase-immunoreactive (TH-ir) neurons to colocalize c-Fos in the NSTc. No nitric oxide synthase (NOS)-ir neurons in the NSTc colocalized c-Fos in either distension or control conditions. Local brain stem application (2 ng) of α-adrenoreceptor antagonists (i.e., α1-prazosin or α2-yohimbine) significantly reduced the magnitude of the esophageal distension-induced gastric relaxation to ∼55% of control conditions. The combination of yohimbine and prazosin reduced the magnitude of the reflex to ∼27% of control. In contrast, pretreatment with either the NOS-inhibitor NG-nitro-l-arginine methyl ester or the β-adrenoceptor antagonist propranolol did not interfere with esophageal distension-induced gastric relaxation. Unilateral microinjections of the agonist norepinephrine (0.3 ng) directed at the DMN were sufficient to mimic the transient esophageal-gastric reflex. Our data suggest that noradrenergic, but not nitrergic, neurons of the NSTc play a prominent role in the modulation of the RRR through action on α1- and α2-adrenoreceptors. The finding that esophageal afferent stimulation alone is not sufficient to activate NOS-positive neurons in the NSTc suggests that these neurons may be strongly gated by other central nervous system inputs, perhaps related to the coordination of swallowing or emesis with respiration.

Glutamatergic plasticity within neurocircuits of the dorsal vagal complex and the regulation of gastric functions

2021 ◽  
Author(s):  
Courtney Clyburn ◽  
Kirsteen N Browning
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Intestinal Secretion ◽  
Motor Nucleus ◽  
Glutamatergic Transmission ◽  
Gi Tract ◽  
Dorsal Motor Nucleus ◽  
Efferent Neurons ◽  
Rapid Transmission

The meticulous regulation of the gastrointestinal (GI) tract is required for the co-ordination of gastric motility and emptying, intestinal secretion, absorption, and transit as well as for the overarching management of food intake and energy homeostasis. Disruption of GI functions is associated with the development of severe GI disorders as well as the alteration of food intake and caloric balance. Functional GI disorders as well as the dysregulation of energy balance and food intake are frequently associated with, or result from, alterations in the central regulation of GI control. The faithful and rapid transmission of information from the stomach and upper GI tract to second order neurons of the nucleus of the tractus solitarius (NTS) relies on the delicate modulation of excitatory glutamatergic transmission, as does the relay of integrated signals from the NTS to parasympathetic efferent neurons of the dorsal motor nucleus of the vagus (DMV). Many studies have focused on understanding the physiological and pathophysiological modulation of these glutamatergic synapses, although their role in the control and regulation of GI functions has lagged behind that of cardiovascular and respiratory functions. The purpose of this review is to examine the current literature exploring the role of glutamatergic transmission in the DVC in the regulation of Gl functions.

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.

scholarly journals Norepinephrine effects on identified neurons of the rat dorsal motor nucleus of the vagus

2004 ◽  
Vol 286 (2) ◽  
pp. G333-G339 ◽  
Author(s):  
Isabel Martinez-Peña y Valenzuela ◽  
Richard C. Rogers ◽  
Gerlinda E. Hermann ◽  
R. Alberto Travagli
Keyword(s):  
Tyrosine Hydroxylase ◽  
Action Potential ◽  
Specific Pattern ◽  
Lower Percentage ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
Thin Slices ◽  
Immunohistochemical Techniques ◽  
Kinetics Of ◽  
Whole Cell Recordings

The dorsal motor nucleus of the vagus (DMV) receives more noradrenergic terminals than any other medullary nucleus; few studies, however, have examined the effects of norepinephrine (NE) on DMV neurons. Using whole cell recordings in thin slices, we determined the effects of NE on identified gastric-projecting DMV neurons. Twenty-five percent of DMV neurons were unresponsive to NE, whereas the remaining 75% responded to NE with either an excitation (49%), an inhibition (26%), or an inhibition followed by an excitation (4%). Antrum/pylorus- and corpus-projecting neurons responded to NE with a similar percentage of excitatory (49 and 59%, respectively) and inhibitory (20% for both groups) responses. A lower percentage of excitatory (37%) and a higher percentage of inhibitory (36%) responses were, however, observed in fundus-projecting neurons. In all groups, pretreatment with prazosin or phenylephrine antagonized or mimicked the NE-induced excitation, respectively. Pretreatment with yohimbine or UK-14304 antagonized or mimicked the NE-induced inhibition, respectively. These data suggest that NE depolarization is mediated by α1-adrenoceptors, whereas NE hyperpolarization is mediated by α2-adrenoceptors. In 16 neurons depolarized by NE, amplitude of the action potential afterhyperpolarization (AHP) and its kinetics of decay (τ) were significantly reduced vs. control. No differences were found on the amplitude and τ of AHP in neurons hyperpolarized by NE. Using immunohistochemical techniques, we found that the distribution of tyrosine hydroxylase fibers within the DMV was significantly different within the mediolateral extent of DMV; however, distribution of cells responding to NE did not show a specific pattern of localization.

scholarly journals A Few TH-Immunoreactive Neurons Closely Appose DMX-Located Neuronal Somata Projecting to the Stomach Prepyloric Region in the Pig

Animals ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 2008
Author(s):  
Jaroslaw Calka ◽  
Marta Ganko ◽  
Andrzej Rychlik
Keyword(s):  
Vagus Nerve ◽  
Spatial Relationship ◽  
Regulatory Action ◽  
Motor Nucleus ◽  
Neuronal Somata ◽  
Fast Blue ◽  
Retrograde Tracer ◽  
Dorsal Motor Nucleus ◽  
Efferent Neurons ◽  
Functional Control

The vagus nerve is responsible for efferent innervation and functional control of stomach functions. The efferent fibers originate from neurons located in the dorsal motor nucleus of the vagus (DMX) and undergo functional control of the local neuroregulatory terminals. The aim of the present study was to examine the existence of morphological foundations for direct regulatory action of the local TH-immunoreactive neurons on parasympathetic efferent neurons supplying the prepyloric region of the porcine stomach. Combined injection of neuronal retrograde tracer Fast Blue into the stomach prepyloric region with TH immunostaining was used in order to visualize spatial relationship between DMX-located stomach prepyloric region supplying neuronal stomata and local TH-IR terminals. We confirmed existence of TH-immunoreactive neural terminals closely opposing the stomach prepyloric region innervating neurons at the porcine DMX area. The observed spatial relationship points out the possibility of indirect catecholaminergic control of the stomach function exerted through preganglionic parasympathetic efferent neurons in the pig.

scholarly journals Catecholaminergic neurons in rat dorsal motor nucleus of vagus project selectively to gastric corpus

2001 ◽  
Vol 280 (3) ◽  
pp. G361-G367 ◽  
Author(s):  
Jinfeng J. Guo ◽  
Kirsteen N. Browning ◽  
Richard C. Rogers ◽  
R. Alberto Travagli
Keyword(s):  
Gastric Fundus ◽  
Gastric Distension ◽  
Motor Nucleus ◽  
Catecholaminergic Neurons ◽  
Dorsal Motor Nucleus ◽  
Balloon Distension ◽  
Esophageal Balloon ◽  
Gastric Corpus ◽  
Oxide Synthase ◽  
The Brain

Nitric oxide synthase-immunoreactive (NOS-IR) neurons in the rat caudal dorsal motor nucleus of the vagus (DMV) project selectively to the gastric fundus and may be involved in vagal reflexes controlling gastric distension. This study aimed to identify the gastric projections of tyrosine hydroxylase-immunoreactive (TH-IR) DMV neurons, whether such neurons colocalize NOS-IR, and if they are activated after esophageal distension. Gastric-projecting neurons were identified after injection of retrograde tracers into the muscle wall of the gastric fundus, corpus, or antrum/pylorus before removal and processing of the brain stems for TH- and NOS-IR. A significantly higher proportion of corpus- compared with fundus- and antrum/pylorus-projecting neurons were TH-IR (14% compared with 4% and 2%, respectively, P < 0.05). Colocalization of NOS- and TH-IR was never observed in gastric-projecting neurons. In rats tested for c-Fos activation after intermittent esophageal balloon distension, no colocalization with TH-IR was observed in DMV neurons. These findings suggest that TH-IR neurons in the caudal DMV project mainly to the gastric corpus, constitute a subpopulation distinct from that of nitrergic vagal neurons, and are not activated on esophageal distension.

Control of lower esophageal sphincter pressure by two sites in dorsal motor nucleus of the vagus

1990 ◽  
Vol 259 (6) ◽  
pp. G899-G906 ◽  
Author(s):  
C. D. Rossiter ◽  
W. P. Norman ◽  
M. Jain ◽  
P. J. Hornby ◽  
S. Benjamin ◽  
...  
Keyword(s):  
Glutamic Acid ◽  
Lower Esophageal Sphincter ◽  
Lower Esophageal Sphincter Pressure ◽  
Motor Nucleus ◽  
Sphincter Pressure ◽  
Intragastric Pressure ◽  
Dorsal Motor Nucleus ◽  
Efferent Neurons ◽  
Esophageal Sphincter ◽  
Pyloric Motility

Our purpose was to determine the central vagal sites for regulating changes in lower esophageal sphincter (LES) pressure in the cat. Injection of the retrograde tracer, horseradish peroxidase, into the LES resulted in labeling of cells in the dorsal motor nucleus of the vagus (DMV), with the largest number of cells appearing in two areas, one area rostral to obex (1.5-4.0 mm) and one area caudal to obex (-0.5 to -1.5 mm). In alpha-chloralose-anesthetized cats, L-glutamic acid was microinjected into these areas and LES pressure, intragastric pressure, and stomach motility were monitored. Microinjection of L-glutamic acid into the rostral area resulted in significant increases in LES pressure (18.6 +/- 4.9 mmHg; P less than 0.05), pyloric motility (baseline minute motility increased from 5.7 +/- 2.2 to 14.5 +/- 3.9 postinjection; P less than 0.05) and stomach pressure (baseline of 16.9 +/- 2.3 mmHg increased to 23.8 +/- 3.7 mmHg postinjection; P less than 0.05). Microinjection of L-glutamic acid into the caudal area resulted in significant decreases in LES pressure (-14.3 +/- 5.8 mmHg; P less than 0.05) and intragastric pressure (-7.5 +/- 2.2 mmHg; P less than 0.05) with no significant changes in pyloric motility. Ipsilateral vagotomy abolished both sets of responses. These data indicate that excitatory and inhibitory control of LES and intragastric pressure are mediated by vagal efferent neurons located in two distinct sites in the DMV.

Functional evidence for the presence of nitric oxide synthase in the dorsal motor nucleus of the vagus

1995 ◽  
Vol 109 (5) ◽  
pp. 1484-1491 ◽  
Author(s):  
William H. Panico ◽  
Nicholas John Cavuto ◽  
George Kallimanis ◽  
Cuong Nguyen ◽  
David M. Armstrong ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
Oxide Synthase

Glucose does not activate nonadrenergic, noncholinergic inhibitory neurons in the rat stomach

2005 ◽  
Vol 288 (3) ◽  
pp. R742-R750 ◽  
Author(s):  
Min Shi ◽  
Allison R. Jones ◽  
Manuel Ferreira ◽  
Niaz Sahibzada ◽  
Richard A. Gillis ◽  
...  
Keyword(s):  
Gastric Motility ◽  
No Reduction ◽  
Cholinergic Neurons ◽  
Inhibitory Neurons ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
The Central Nervous System ◽  
Fos Expression ◽  
Oxide Synthase

We reported previously that intravenously administered d-glucose acts in the central nervous system to inhibit gastric motility induced by hypoglycemia in anesthetized rats. The purpose of this study was to determine whether this effect is due to inhibition of dorsal motor nucleus of the vagus (DMV) cholinergic motoneurons, which synapse with postganglionic cholinergic neurons, or to excitation of DMV cholinergic neurons, which synapse with postganglionic nonadrenergic, noncholinergic (NANC) neurons, particularly nitrergic neurons. Three approaches were employed: 1) assessment of the efficacy of d-glucose-induced inhibition of gastric motility in hypoglycemic rats with and without inhibition of nitric oxide synthase [10 mg/kg iv nitro-l-arginine methyl ester (l-NAME)], 2) assessment of the efficacy of intravenous bethanechol (30 μg·kg−1·min−1) to stimulate gastric motility in hypoglycemic rats during the time of d-glucose-induced inhibition of gastric motility, and 3) determination of c-Fos expression in DMV neurons after intravenous d-glucose was administered to normoglycemic rats. Results obtained demonstrated that l-NAME treatment had no effect on d-glucose-induced inhibition of gastric motility; there was no reduction in the efficacy of intravenous bethanechol to increase gastric motility, and c-Fos expression was not induced by d-glucose in DMV neurons that project to the stomach. These findings indicate that excitation of DMV cholinergic motoneurons that synapse with postganglionic NANC neurons is not a significant contributing component of d-glucose-induced inhibition of gastric motility.

scholarly journals Nitric oxide synthase in motor neurons after axotomy.

1994 ◽  
Vol 42 (4) ◽  
pp. 451-457 ◽  
Author(s):  
W H Yu
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Motor Neurons ◽  
Motor Nucleus ◽  
Spinal Nerves ◽  
Spinal Motor Neurons ◽  
Spinal Motor ◽  
Dorsal Motor Nucleus ◽  
Motor Nuclei ◽  
Oxide Synthase

Nitric oxide synthase (NOS), an enzyme involved in synthesis of nitric oxide (NO), has been localized in many diverse cell types. In the CNS and PNS, discrete neuron cell groups express NOS constitutively. Recent evidence indicates that NOS is inducible in neurons normally not expressing NOS. After transection of peripheral nerves, NOS expression was significantly up-regulated in the axotomized sensory ganglion cells, whereas in the corresponding motor neurons NOS was not induced unless axon regeneration was prevented and ensuing neuron death became massive. Studies on axotomy-induced NOS have been limited largely to spinal nerves, with only one reported in the vagus nerve. The aim of this study was to determine whether NOS induction in motor neurons of the brainstem after axotomy is regulated in a manner similar to that of the spinal cord. By NADPH-diaphorase histochemistry and NOS immunocytochemistry, the status of NOS in neurons of the hypoglossal nucleus, dorsal motor nucleus of the vagus, and motor nucleus of the facial nerve was examined 2 weeks after unilateral transection of the respective cranial nerves, and the results were compared with those of spinal motor neurons after transection of the sciatic nerve. NOS, undetectable in neurons of the three cranial motor nuclei of sham-operated animals, was observed in about 30-50% of neurons in the cranial motor nuclei ipsilateral to axotomy, but it was not detected in spinal motor neurons after axotomy. NOS localized in axotomized cranial motor neurons was unrelated to NOS of macrophages or endothelial cells. There was no appreciable cell loss from axotomy at this period except in the dorsal motor nucleus of the vagus, where some loss was observed. The results indicate that there is a fundamental difference in the regulation of NOS expression between motor neurons of the cranial and spinal nerves. The possible role of NOS/NO acting as cytoprotective or cytotoxic agent on injured motor neurons is discussed. Motor neurons of cranial and spinal nerves may serve as a useful model to further define the roles of NOS/NO in neurons, especially after traumatic injury.

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