Gastric branch vagotomy blocks nutrient and cholecystokinin-induced suppression of gastric emptying

1993 ◽  
Vol 264 (3) ◽  
pp. R630-R637 ◽  
Author(s):  
G. J. Schwartz ◽  
G. Berkow ◽  
P. R. McHugh ◽  
T. H. Moran
Keyword(s):  
Gastric Emptying ◽  
Intraperitoneal Administration ◽  
Physiological Saline ◽  
Male Rats ◽  
Caloric Content ◽  
Vagus Nerves ◽  
Acidic Solutions ◽  
Caloric Density ◽  
The Brain

A role for the vagus nerve in the emptying of intragastric nutrients and the gastric inhibitory actions of the brain-gut peptide cholecystokinin (CCK) has been proposed. To directly assess the role of the gastric vagal branches in these actions, we compared the emptying of 5-ml nutrient and nonnutrient gastric loads in male rats in which both branches of the gastric vagus nerves were cut (GVX, n = 7) with emptying in surgical control (n = 8) rats. Gastric emptying of saline was also examined in both groups after intraperitoneal administration of 8 micrograms/kg CCK. In control rats, high osmolarity, low pH, and caloric density all significantly decreased gastric emptying compared with the emptying of physiological saline. In addition, fat (oleic acid) and protein (peptone) loads emptied significantly more slowly than isocaloric carbohydrate (glucose) loads. Gastric branch vagotomy completely blocked the suppression of emptying produced by fat, protein, carbohydrate, and acid loads. In addition, GVX attenuated the ability of hyperosmotic nutrient and nonnutrient loads to inhibit emptying to the same degree, irrespective of their caloric content. Finally, in intact rats, CCK significantly inhibited the emptying of physiological saline, and gastric vagotomy abolished this suppression. Taken together, these results are consistent with the proposals that 1) the controlled emptying of caloric, hyperosmotic, and acidic solutions is dependent on gastric vagal branches, and 2) exogenous CCK relies on an intact vagal pathway in the control of gastric emptying.

Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

2009 ◽  
Vol 296 (3) ◽  
pp. R587-R594 ◽  
Author(s):  
Premysl Bercik ◽  
Elena F. Verdú ◽  
Jane A. Foster ◽  
Jun Lu ◽  
Angela Scharringa ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Feeding Behavior ◽  
Computer Assisted ◽  
Bacterial Eradication ◽  
Cell Counts ◽  
Tnf Α ◽  
Gastric Sensitivity ◽  
H Pylori ◽  
The Brain

Bacterial infection can trigger the development of functional GI disease. Here, we investigate the role of the gut-brain axis in gastric dysfunction during and after chronic H. pylori infection. Control and chronically H. pylori-infected Balb/c mice were studied before and 2 mo after bacterial eradication. Gastric motility and emptying were investigated using videofluoroscopy image analysis. Gastric mechanical viscerosensitivity was assessed by cardioautonomic responses to distension. Feeding patterns were recorded by a computer-assisted system. Plasma leptin, ghrelin, and CCK levels were measured using ELISA. IL-1β, TNF-α, proopiomelanocortin (POMC), and neuropeptide Y mRNAs were assessed by in situ hybridizations on frozen brain sections. Gastric inflammation was assessed by histology and immunohistochemistry. As shown previously, H. pylori-infected mice ate more frequently than controls but consumed less food per bout, maintaining normal body weight. Abnormal feeding behavior was accompanied by elevated plasma ghrelin and postprandial CCK, higher TNF-α (median eminence), and lower POMC (arcuate nucleus) mRNA. Infected mice displayed delayed gastric emptying and visceral hypersensitivity. Eradication therapy normalized gastric emptying and improved gastric sensitivity but had no effect on eating behavior. This was accompanied by persistently increased TNF-α in the brain and gastric CD3+ T-cell counts. In conclusion, chronic H. pylori infection in mice alters gastric emptying and mechanosensitivity, which improve after bacterial eradication. A feeding pattern reminiscent of early satiety persists after H. pylori eradication and is accompanied by increased TNF-α in the brain. The results support a role for altered gut-brain pathways in the maintenance of postinfective gut dysfunction.

Endogenous cholecystokinin in the control of gastric emptying of liquid nutrient loads in rhesus monkeys

1993 ◽  
Vol 265 (2) ◽  
pp. R371-R375 ◽  
Author(s):  
T. H. Moran ◽  
P. J. Ameglio ◽  
G. J. Schwartz ◽  
H. J. Peyton ◽  
P. R. McHugh
Keyword(s):  
Gastric Emptying ◽  
Rhesus Monkeys ◽  
Physiological Saline ◽  
Inhibitory Effect ◽  
Intragastric Administration ◽  
Nutrient Loads ◽  
Cck Receptor Antagonist ◽  
Quantitative Contribution ◽  
The Brain ◽  
Cck Antagonist

A role for the brain/gut peptide cholecystokinin (CCK) in the control of gastric emptying has been proposed. In the present studies, we have used a potent type A CCK-receptor antagonist (devazepide) to examine the quantitative contribution of endogenously released CCK in the control of liquid gastric emptying of 100 ml lipid, protein, and carbohydrate test loads in rhesus monkeys. Emptying was studied in conscious monkeys equipped with chronic indwelling gastric cannulas. Prior intragastric administration of devazepide (1.0-320 micrograms/kg) differentially affected the 10-min emptying of glucose (0.125/ml), peptone (4.5%), and Intralipid (4.5%). Glucose emptying was not affected by any dose of the CCK antagonist. The emptying of peptone was accelerated by doses of 10 micrograms/kg or higher. This effect, however, was only partial and plateaued at a dose of 100 micrograms/kg. The gastric emptying of Intralipid was accelerated at a dose of 32 micrograms/kg, and the inhibitory effect of the Intralipid was completely eliminated at a dose of 320 micrograms/kg. At this dose of devazepide, the Intralipid test meal emptied from the stomach at the same rate as physiological saline. These data demonstrate that in rhesus monkeys endogenously released CCK 1) does not play a role in the control of glucose emptying, 2) is a partial mediator of the inhibitory action of peptone on gastric emptying, and 3) is the primary inhibitory mediator in the control of the gastric emptying of Intralipid.

scholarly journals A Possible Mechanism for the Action of Adrenomedullin in Brain to Stimulate Stress Hormone Secretion

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 4890-4896 ◽  
Author(s):  
Meghan M. Taylor ◽  
Willis K. Samson
Keyword(s):  
Hpa Axis ◽  
Hormone Secretion ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Stress Hormone ◽  
Elevated Plasma ◽  
The Central Nervous System ◽  
Neuroendocrine Responses ◽  
The Brain

Abstract Adrenomedullin (AM) has been reported to have actions at each level of the hypothalamo-pituitary-adrenal (HPA) axis, suggesting that the peptide plays a role in the organization of the neuroendocrine responses to stress. We examined the mechanism by which AM regulates the central nervous system branch of the HPA axis as well as the possible role of AM in the modulation of the releases of two other hormones, prolactin and GH, whose secretions also are altered by stress. Intracerebroventricular administration of AM led to elevated plasma corticosterone levels in unrestrained, conscious male rats. This effect was abrogated by pretreatment with a CRH antagonist, suggesting that AM activates the HPA axis by causing the release of CRH into hypophyseal portal vessels. In addition, AM given intracerebroventricularly stimulated the release of prolactin but did not alter the secretion of GH. We propose that AM produced in the brain may be an important neuromodulator of the hormonal stress response.

scholarly journals EXPERIMENTAL INVESTIGATION ON CARBACETAM INFLUENCE ON HYPOTHALAMUS TISSUE IN BRAIN INJURY

2018 ◽  
Vol 14 (1-2) ◽  
pp. 11-17
Author(s):  
S.V. Ziablytsev ◽  
T.I. Panova ◽  
O.O. Starodubska ◽  
O.O. Dyadik
Keyword(s):  
Brain Injury ◽  
Physiological Saline ◽  
Neuroendocrine Cells ◽  
Nerve Tissue ◽  
Male Rats ◽  
Control Group ◽  
S 100 ◽  
Hypothalamic Tissue ◽  
Hematoxylin And Eosin ◽  
The Brain

Relevance. A key role in the pathogenesis of the brain injury is played by destructive changes in the hypothalamus neuroendocrine cells. For the correction of such disorders, promising is carbacetam, which has antihypoxic, anti-edema and anti-shock effects. Objective: to investigate the effect of carbacetam on the processes of neurodegeneration in the paraventricular and supraoptical nuclei of the hypothalamus in the experimental brain injury. Material and methods. Brain injury were modeled on the V.M. Elskyy &S.V. Ziablitsev model on white non-breeding male rats weighing 200±10 g. Experimental animals (n=10) received intraabdominal injection of carbacetam at a dose of 5 mg/kg in 1 ml of physiological saline during the seven days after injury. In the control group (n=10), 1 ml of physiological saline was injected. Hypothalamic tissue microparticles performed a morphological and immunohistochemical evaluation of neurodegenerative changes when stained with hematoxylin and eosin and immunohistochemically to detect NSE, S-100 and GFAP neuromarkers. Results. Carbacetam reduced the degenerative processes in the nervous tissue of the paraventricular and supraoptical nuclei of the hypothalamus, which was manifested by the restoration of normal morphological features, in contrast to rats that did not receive the drug. Immunohistochemically, GFAP and S-100 glial markers exhibited reduced, reflecting a reduction in degenerative changes in the nerve tissue. Expressions of the neurons marker NSE increased, reflecting high metabolic activity of the neurons. Conclusions. Revealed changes in the expression of markers of neurons and glia showed a restoration of normal neuronal activity due to the introduction of carbacetam.

scholarly journals Evaluation on the Pharmacological Effect of Traditional Chinese Medicine SiJunZiTang on Stress-Induced Peptic Ulcers

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Chiu-Mei Chen ◽  
Chien-Ying Lee ◽  
Po-Jung Lin ◽  
Chin-Lang Hsieh ◽  
Hung-Che Shih
Keyword(s):  
Chinese Medicine ◽  
Control Group ◽  
Therapeutic Effects ◽  
Total Acidity ◽  
Peptic Ulcers ◽  
Vagus Nerves ◽  
Cure Rate ◽  
Central Neurotransmitters ◽  
The Brain

Purpose. To explore the effects of SiJunZiTang (SJZT) on central neurotransmitters and the inhibition of HCl hypersecretion, along with the role of the vagus nerve. From this, the effects of SJZT and its constituent ingredients on inhibiting stress-induced peptic ulcers will be determined.Methods. Methods used to determine SJZT's effectiveness included (1) measuring the antipeptic ulcer effects of varying combinations of the constituents of SJZT; (2) evaluations of monoamine (MA) level in the brain; and (3) measuring the effects of longer-term SJZT treatment.Results. Comparing the control and experimental groups where the rats’ vagus nerves were not cut after taking SJZT orally (500 mg/kg and 1000 mg/kg), the volume of enterogastric juice, free HCl and total acidity all reduce dose-dependently. The group administered SJZT at 1000 mg/kg showed significant reductions (P<0.05). For the experimental groups where the vagus nerves were cut, a comparison with the control group suggests that the group receiving SJZT (500 mg/kg) orally for 21 days demonstrated a cure rate of 34.53%.Conclusion. The results display a correlation between the therapeutic effects of SJZT on stress-induced peptic ulcers and central neurotransmitter levels. Further to this, SJZT can inhibit the hypersecretion of HCl in the stomach, thus inhibiting stress-induced peptic ulcers.

scholarly journals Importance of the Paraventricular Nucleus of the Hypothalamus as a Component of a Neural Pathway between the Brain and the Testes that Modulates Testosterone Secretion Independently of the Pituitary

Endocrinology ◽  
2003 ◽  
Vol 144 (2) ◽  
pp. 594-598 ◽  
Author(s):  
Daniel J. Selvage ◽  
Catherine Rivier
Keyword(s):  
Paraventricular Nucleus ◽  
Leydig Cell ◽  
Pseudorabies Virus ◽  
Cell Function ◽  
Brain Area ◽  
Male Rats ◽  
Neural Pathway ◽  
Electrolytic Lesions ◽  
The Brain

We previously reported that in adult male rats, the intracerebroventricular (icv) injection of corticotropin-releasing factor (CRF) or the β-adrenergic agonist isoproterenol (ISO) significantly inhibited the ability of human chorionic gonadotropin (hCG) to stimulate testosterone (T) secretion. The finding that this phenomenon also took place when LH release had been blocked with an LHRH antagonist suggested that icv CRF and ISO did not alter Leydig cell function by influencing the activity of pituitary gonadotrophs. We therefore proposed the existence of a neural pathway connecting the brain to the testes, whose activation by icv CRF or ISO interfered with T secretion. Based on the intratesticular injection of the transganglionic tracer pseudorabies virus, we recently identified the paraventricular nucleus (PVN) of the hypothalamus as a component of this neural link. The aim of the present work was to investigate the functional role of this brain area in mediating the ability of CRF and ISO to inhibit the ability of hCG to stimulate T secretion. We first demonstrated that local microinfusion of CRF or ISO directly into the PVN mimicked the effect of their icv injection, suggesting that the PVN does indeed represent a site of action of ISO and CRF in altering Leydig cell responsiveness to gonadotropin. In contrast, neither CRF nor ISO microinfusion into the central amygdala or the frontal cortex influenced hCG-stimulated T secretion. To further investigate the role of the PVN in ISO- and CRF-induced blunting of hCG stimulation of T, we determined the effect of icv CRF or ISO on testicular activity of rats with electrolytic lesions of the PVN. These lesions, which did not in themselves influence Leydig cell responsiveness to hCG, blocked the effect of both icv ISO and CRF on hCG-induced T release. Collectively, these results support the hypothesis that CRF- and ISO-induced activation of cells in the area of the PVN decreases the ability of gonadotropin to release T and suggests that this nucleus represents an important site of the proposed neural connection between the brain and the testes.

scholarly journals The effects of 6 hours of hypoxia on protein synthesis in rat tissues in vivo and in vitro

1985 ◽  
Vol 228 (1) ◽  
pp. 179-185 ◽  
Author(s):  
V R Preedy ◽  
D M Smith ◽  
P H Sugden
Keyword(s):  
Protein Synthesis ◽  
Gastric Emptying ◽  
Skeletal Muscles ◽  
Rat Tissues ◽  
Tissue Nitrogen ◽  
The Brain ◽  
H Protein

Rates of protein synthesis were measured in vivo in several tissues (heart, skeletal muscles, liver, tibia, skin, brain, kidney, lung) of fed rats exposed to O2/N2 (1:9) for 6 h starting at 08:00-11:00 h. Protein synthesis rates were depressed by 15-35% compared with normoxic controls in all of the tissues studied. The decreases were greatest in the brain and the skin. Although hypoxia inhibited gastric emptying, its effects on protein synthesis could probably not be attributed to its induction of a starved state, because protein-synthesis rates in brain and skin were not decreased by a 15-18 h period of starvation initiated at 23:00 h. Furthermore, we showed that protein synthesis was inhibited by hypoxia in the rat heart perfused in vitro, suggesting a direct effect. The role of hypoxia in perturbing tissue nitrogen balance in various physiological and pathological states is discussed.

scholarly journals Sites and sources of sympathoexcitation in obese male rats: role of brain insulin

2020 ◽  
Vol 318 (3) ◽  
pp. R634-R648 ◽  
Author(s):  
Zhigang Shi ◽  
Ding Zhao ◽  
Priscila A. Cassaglia ◽  
Virginia L. Brooks
Keyword(s):  
Insulin Receptors ◽  
Male Rats ◽  
Melanocortin Receptor ◽  
Sprague Dawley ◽  
Intracerebroventricular Infusion ◽  
Sprague Dawley Rats ◽  
Y1 Receptors ◽  
The Brain ◽  
Obese Male

In males, obesity increases sympathetic nerve activity (SNA), but the mechanisms are unclear. Here, we investigate insulin, via an action in the arcuate nucleus (ArcN), and downstream neuropathways, including melanocortin receptor 3/4 (MC3/4R) in the hypothalamic paraventricular nucleus (PVN) and dorsal medial hypothalamus (DMH). We studied conscious and α-chloralose-anesthetized Sprague-Dawley rats fed a high-fat diet, which causes obesity prone (OP) rats to accrue excess fat and obesity-resistant (OR) rats to maintain fat content, similar to rats fed a standard control (CON) diet. Nonspecific blockade of the ArcN with muscimol and specific blockade of ArcN insulin receptors (InsR) decreased lumbar SNA (LSNA), heart rate (HR), and mean arterial pressure (MAP) in OP, but not OR or CON, rats, indicating that insulin supports LSNA in obese males. In conscious rats, intracerebroventricular infusion of insulin increased MAP only in OP rats and also improved HR baroreflex function from subnormal to supranormal. The brain sensitization to insulin may elucidate how insulin can drive central SNA pathways when transport of insulin across the blood-brain barrier may be impaired. Blockade of PVN, but not DMH, MC3/4R with SHU9119 decreased LSNA, HR, and, MAP in OP, but not OR or CON, rats. Interestingly, nanoinjection of the MC3/4R agonist melanotan II (MTII) into the PVN increased LSNA only in OP rats, similar to PVN MTII-induced increases in LSNA in CON rats after blockade of sympathoinhibitory neuropeptide Y Y1 receptors. ArcN InsR expression was not increased in OP rats. Collectively, these data indicate that obesity increases SNA, in part via increased InsR signaling and downstream PVN MC3/4R.

scholarly journals Molecular and cellular mechanisms of central nervous system alteration in COVID-19

2020 ◽  
Vol 9 (3) ◽  
pp. 72-85
Author(s):  
N. T. Alexeeva ◽  
D. A. Sokolov ◽  
D. B. Nikityuk ◽  
S. V. Klochkova ◽  
A. G. Kvaratskheliya
Keyword(s):  
Immune Cells ◽  
Defense Mechanisms ◽  
Retrograde Axonal Transport ◽  
Antiviral Defense ◽  
Vagus Nerves ◽  
Cellular Mechanisms ◽  
Inflammatory Reactions ◽  
Viral Particles ◽  
The Brain

The ongoing coronavirus disease 2019 (COVID-19) pandemic dictates the need to study the molecular and cellular mechanisms of interaction between the pathogen and the human body. The manifestation of neurological symptoms in some patients with COVID-19 is a problem for neuroscientists due to the insufficiently understood pathomorphogenesis of the disease. This review systematizes the literature data reflecting the ways of penetration of SARS-CoV-2 into the brain, features of its interaction with neurons, neuroglia, and immune cells. It has been shown that the main mechanisms of SARS-CoV-2 neuroinvasion are presumably retrograde axonal transport along the fibers of the olfactory and vagus nerves; penetration through the damaged blood-brain barrier (BBB) or migration of immunocompetent cells containing viral particles through the intact BBB. It was found that virusinducible neuronal death is caused not only by a direct cytotoxic effect, but also due to dysregulation of the reninangiotensin system of the brain and the release of a large amount of inflammatory cytokines as a manifestation of a “cytokine storm”. The participation of neuroglial cells in the initiation and maintenance of neuroinflammatory and neurodegenerative processes due to the activation of their proinflammatory phenotype has been demonstrated. The role of mast cells in antiviral defense mechanisms and inflammatory reactions is discussed.

26. Investigating the Role of Neuropeptide Y Infusions to the Ventral Hippocampus in Mediating Defensive Burying Behavior in Rats in the Shock-Probe Test

2018 ◽  
Author(s):  
Samuel Yoon
Keyword(s):  
Animal Model ◽  
Neuropeptide Y ◽  
Selective Reduction ◽  
Physiological Saline ◽  
Ventral Hippocampus ◽  
Defensive Behaviors ◽  
Probe Test ◽  
Defensive Burying ◽  
The Brain

The current study will investigate the role of NPY in the ventral hippocampus in anxiety. NPY is a neuropeptide found in many structures in the brain, including the hippocampus, and is implicated in regulation of anxiety related behaviors. The hippocampus has also been found to play a role in anxiety and defensive behaviors – specifically, the ventral hippocampus regulates innate defensive behaviors. The effect of NPY in the ventral hippocampus will be investigated by infusing either NPY (n=12) or physiological saline (n=12) into the rat ventral hippocampus followed by behavioural testing in an animal model of anxiety; i.e., the shock-probe burying task. I expect to find a selective reduction in burying duration in NPY-infused rats.

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