Prior vagotomy blocks VMH obesity in pair-fed rats

1981 ◽  
Vol 240 (5) ◽  
pp. E573-E583 ◽  
Author(s):  
J. E. Cox ◽  
T. L. Powley
Keyword(s):  
Food Intake ◽  
Cell Loss ◽  
Ventromedial Hypothalamus ◽  
Motor Nucleus ◽  
Previous Suggestion ◽  
Hypothalamic Obesity ◽  
Dorsal Motor Nucleus ◽  
Gastric Contents ◽  
Feeding Regimen ◽  
Protein Output

Previously vagotomized, ventromedial hypothalamus (VMH)-lesioned rats and sham-lesioned controls were maintained on an intragastric pair-feeding regimen in which nonvagotomized VMH rats deposit excessive fat. Hypothalamic lesions were produced after 6 days of adaptation to pair feeding, and the experiment continued for 30 days postlesion. Extent of vagotomy was determined with a multiple-regression procedure with cell loss in the dorsal motor nucleus of the vagus, fasting gastric contents, and basal pancreatic protein output as predictor variables. The correlation was 0.95 between this set of indexes and the adequacy of a vagotomy for preventing hypothalamic obesity. Thus, radical vagotomies precluded the typical accumulation of significantly increased levels of carcass fat in lesioned animals (16.3 vs. 14.0% for controls). VMH rats with less extensive transections accumulated substantially more fat (25.9%). This outcome suggests that vagotomy produces a specific blockade of lesion-produced disturbances in metabolism leading to obesity. It fails to support a previous suggestion that vagal section blocks VMH obesity merely as a nonspecific surgical restriction of food intake because vagotomy was effective even though its effects on food intake could not operate.

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.

scholarly journals Modulation of food intake by mTOR signalling in the dorsal motor nucleus of the vagus in male rats: focus on ghrelin and nesfatin-1

2013 ◽  
Vol 98 (12) ◽  
pp. 1696-1704 ◽  
Author(s):  
Weizhen Zhang ◽  
Chao Zhang ◽  
Danielle Fritze ◽  
Biaoxin Chai ◽  
Jiyao Li ◽  
...  
Keyword(s):  
Food Intake ◽  
Male Rats ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
Mtor Signalling

scholarly journals Central Neurocircuits Regulating Food Intake in Response to Gut Inputs—Preclinical Evidence

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 908
Author(s):  
Kirsteen N. Browning ◽  
Kaitlin E. Carson
Keyword(s):  
Food Intake ◽  
Vagus Nerve ◽  
Sensory Information ◽  
Specific Reference ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
The Central Nervous System ◽  
Complex Integration ◽  
The Many

The regulation of energy balance requires the complex integration of homeostatic and hedonic pathways, but sensory inputs from the gastrointestinal (GI) tract are increasingly recognized as playing critical roles. The stomach and small intestine relay sensory information to the central nervous system (CNS) via the sensory afferent vagus nerve. This vast volume of complex sensory information is received by neurons of the nucleus of the tractus solitarius (NTS) and is integrated with responses to circulating factors as well as descending inputs from the brainstem, midbrain, and forebrain nuclei involved in autonomic regulation. The integrated signal is relayed to the adjacent dorsal motor nucleus of the vagus (DMV), which supplies the motor output response via the efferent vagus nerve to regulate and modulate gastric motility, tone, secretion, and emptying, as well as intestinal motility and transit; the precise coordination of these responses is essential for the control of meal size, meal termination, and nutrient absorption. The interconnectivity of the NTS implies that many other CNS areas are capable of modulating vagal efferent output, emphasized by the many CNS disorders associated with dysregulated GI functions including feeding. This review will summarize the role of major CNS centers to gut-related inputs in the regulation of gastric function with specific reference to the regulation of food intake.

scholarly journals Regulation of food intake by astrocytes in the brainstem dorsal vagal complex

2019 ◽  
Author(s):  
Alastair J. MacDonald ◽  
Fiona E. Holmes ◽  
Craig Beall ◽  
Anthony E. Pickering ◽  
Kate L.J. Ellacott
Keyword(s):  
Food Intake ◽  
Area Postrema ◽  
Active Role ◽  
Brain Regions ◽  
Negative Energy ◽  
Motor Nucleus ◽  
Dorsal Vagal Complex ◽  
Structural Support ◽  
Dorsal Motor Nucleus ◽  
Hypothalamic Arcuate Nucleus

Food intake is controlled by the coordinated action of numerous brain regions but a complete understanding remains elusive. Of these brain regions the brainstem dorsal vagal complex (DVC) is the first site for integration of visceral synaptic and hormonal cues that act to inhibit food intake. The DVC consists of three nuclei: the nucleus of the solitary tract (NTS), area postrema (AP) and dorsal motor nucleus of the vagus (DMX). Targeted chemogenetic activation of appetite-responsive NTS neuronal populations causes short term decreases in food intake. Astrocytes are a class of glial cell which provide metabolic and structural support to neurons and play an active role in modulating neurotransmission. Within the hypothalamic arcuate nucleus (ARC) astrocytes are regulated by both positive and negative energy balance and express receptors for hormones that influence satiety and hunger. Chemogenetic activation of these ARC astrocytes alters food intake. Since NTS astrocytes respond to vagal stimulation, we hypothesised that they may be involved in mediating satiety. Here we show that NTS astrocytes show plastic alterations in morphology following excess food consumption and that chemogenetic activation of DVC astrocytes causes a decrease in food intake, by recruiting an appetite-inhibiting circuit, without producing aversion. These findings are the first using genetically-targeted manipulation of DVC astrocytes to demonstrate their role in the brain’s regulation of food intake.

scholarly journals The Role of the Dorsal Vagal Complex and the Vagus Nerve in Feeding Effects of Melanocortin-3/4 Receptor Stimulation*

Endocrinology ◽  
2000 ◽  
Vol 141 (4) ◽  
pp. 1332-1337 ◽  
Author(s):  
Diana L. Williams ◽  
Joel M. Kaplan ◽  
Harvey J. Grill
Keyword(s):  
Food Intake ◽  
Vagus Nerve ◽  
Messenger Rna ◽  
Motor Nucleus ◽  
Dorsal Vagal Complex ◽  
Dorsal Motor Nucleus ◽  
Ventricular Response ◽  
Feeding Effects ◽  
Diet Intake

Abstract Fourth intracerebroventricular (4th-icv) administration of the melanocortin-3/4 receptor (MC3/4-R) agonist, MTII, reduces food intake; the antagonist, SHU9119, increases feeding. The dorsal motor nucleus of the vagus nerve (DMX) contains the highest density of MC4-R messenger RNA in the brain. To explore the possibility that the DMX contributes to 4th-icv MC4-R effects, we delivered doses of MTII and SHU9119 that are subthreshold for ventricular response unilaterally through a cannula centered above the DMX. MTII markedly suppressed 2-h (50%), 4-h (50%), and 24-h (33%) intake. Feeding was significantly increased 4 h (50%) and 24 h (20%) after SHU9119 injections. These results suggest that receptors in the DMX, or the dorsal vagal complex more generally, underlie effects obtained with 4th-icv administration of these ligands. We investigated possible vagal mediation of 4th-icv MTII effects by giving the agonist to rats with subdiaphragmatic vagotomy. MTII suppressed 2-, 4-, and 24-h liquid diet intake (∼80%) to the same extent in vagotomized and surgical control rats. We conclude that stimulation or antagonism of MC3/4-Rs in the dorsal vagal complex yields effects on food intake that do not require an intact vagus nerve.

scholarly journals NMDA Receptor-Dependent Synaptic Activity in Dorsal Motor Nucleus of Vagus Mediates the Enhancement of Gastric Motility by Stimulating ST36

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Xinyan Gao ◽  
Yongfa Qiao ◽  
Baohui Jia ◽  
Xianghong Jing ◽  
Bin Cheng ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Gastric Motility ◽  
Low Frequency ◽  
Synaptic Activity ◽  
Motor Nucleus ◽  
Dorsal Motor Nucleus ◽  
Vagal Reflex ◽  
Precise Molecular Mechanism ◽  
Lines Of Evidence

Previous studies have demonstrated the efficacy of electroacupuncture at ST36 for patients with gastrointestinal motility disorders. While several lines of evidence suggest that the effect may involve vagal reflex, the precise molecular mechanism underlying this process still remains unclear. Here we report that the intragastric pressure increase induced by low frequency electric stimulation at ST36 was blocked by AP-5, an antagonist of N-methyl-D-aspartate receptors (NMDARs). Indeed, stimulating ST36 enhanced NMDAR-mediated, but not 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propanoic-acid-(AMPA-) receptor-(AMPAR-) mediated synaptic transmission in gastric-projecting neurons of the dorsal motor nucleus of the vagus (DMV). We also identified that suppression of presynapticμ-opioid receptors may contribute to upregulation of NMDAR-mediated synaptic transmission induced by electroacupuncture at ST36. Furthermore, we determined that the glutamate-receptor-2a-(NR2A-) containing NMDARs are essential for NMDAR-mediated enhancement of gastric motility caused by stimulating ST36. Taken together, our results reveal an important role of NMDA receptors in mediating enhancement of gastric motility induced by stimulating ST36.

α-Synuclein pathology in the spinal cords of neurologically asymptomatic aged individuals

Neurology ◽  
2006 ◽  
Vol 66 (7) ◽  
pp. 1100-1102 ◽  
Author(s):  
K. J. Klos ◽  
J. E. Ahlskog ◽  
K. A. Josephs ◽  
H. Apaydin ◽  
J. E. Parisi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Substantia Nigra ◽  
Basal Forebrain ◽  
Locus Ceruleus ◽  
Raphe Nucleus ◽  
Motor Nucleus ◽  
Lewy Neurites ◽  
Dorsal Motor Nucleus ◽  
Asymptomatic Individuals

The authors assessed the frequency of spinal cord α-synuclein pathology in neurologically asymptomatic individuals older than 60 years of age (N = 106). Using α-synuclein immunohistochemistry, nine cases (8%) had incidental Lewy neurites in the intermediolateral column and at least some α-synuclein pathology in the dorsal motor nucleus of the vagus, locus ceruleus, and central raphe nucleus. Sparse α-synuclein pathology was also detected in the substantia nigra, basal forebrain, amygdala, or cortex in all but two cases.

scholarly journals Role of Ventromedial Hypothalamus in Sucrose-Induced Obesity on Metabolic Parameters

2021 ◽  
pp. 097275312110057
Author(s):  
Archana Gaur ◽  
G.K. Pal ◽  
Pravati Pal
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Food Intake ◽  
Ventromedial Hypothalamus ◽  
Female Rats ◽  
Metabolic Parameters ◽  
Male Rats ◽  
Significant Weight Gain ◽  
The Metabolic Syndrome

Background: Obesity is because of excessive fat accumulation that affects health adversely in the form of various diseases such as diabetes, hypertension, cardiovascular diseases, and many other disorders. Our Indian diet is rich in carbohydrates, and hence the sucrose-induced obesity is an apt model to mimic this. Ventromedial hypothalamus (VMH) is linked to the regulation of food intake in animals as well as humans. Purpose: To understand the role of VMHin sucrose-induced obesity on metabolic parameters. Methods: A total of 24 adult rats were made obese by feeding them on a 32% sucrose solution for 10 weeks. The VMH nucleus was ablated in the experimental group and sham lesions were made in the control group. Food intake, body weight, and biochemical parameters were compared before and after the lesion. Results: Male rats had a significant weight gain along with hyperphagia, whereas female rats did not have a significant weight gain inspite of hyperphagia. Insulin resistance and dyslipidemia were seen in both the experimental and control groups. Conclusion: A sucrose diet produces obesity which is similar to the metabolic syndrome with insulin resistance and dyslipidemia, and a VMH lesion further exaggerates it. Males are more prone to this exaggeration.

Sign in / Sign up

Export Citation Format

Share Document