scholarly journals Integrative capacity of the caudal brainstem in the control of food intake

2006 ◽  
Vol 361 (1471) ◽  
pp. 1275-1280 ◽  
Author(s):  
Gary J Schwartz
Keyword(s):  
Food Intake ◽  
Neural Activity ◽  
Molecular Genetic ◽  
Visceral Afferents ◽  
Neural Processing ◽  
Solitary Tract ◽  
Brainstem Nucleus ◽  
Peptide Signals ◽  
Signalling Systems ◽  
Food Consumed

The caudal brainstem nucleus of the solitary tract (NTS) is the initial central nervous system (CNS) terminus for a variety of gastrointestinal mechanical, nutrient chemical and gut peptide signals that limit the amount of food consumed during a meal. It receives neuroanatomical projections from gut vagal and non-vagal visceral afferents that mediate the CNS representation of these meal-stimulated gut feedback signals, and is reciprocally connected to a range of hypothalamic and limbic system sites that play significant roles in the neural processing of meal-related stimuli and in determining food consumption. Neurons in the NTS also contains elements of leptinergic and melanocortinergic signalling systems, presenting the possibility that the brainstem actions of these neuropeptides affect both the NTS processing of meal-stimulated gut afferent neural activity and its behavioural potency. Taken together, these features suggest that the NTS is ideally situated to integrate central and peripheral signals that determine meal size. This manuscript will review recent support from molecular genetic, neurophysiological and immunocytochemical studies that begin to identify and characterize the types of integrative functions performed within the NTS, and highlight the extent to which they are consistent with a causal role for NTS integration of peripheral gut and central neuropeptide signals important in the control of food intake.

scholarly journals Influence of a selective histamine H3 receptor antagonist on hypothalamic neural activity, food intake and body weight

2005 ◽  
Vol 29 (12) ◽  
pp. 1402-1412 ◽  
Author(s):  
K Malmlöf ◽  
F Zaragoza ◽  
V Golozoubova ◽  
H H F Refsgaard ◽  
T Cremers ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Receptor Antagonist ◽  
Neural Activity ◽  
Histamine H3 Receptor ◽  
H3 Receptor ◽  
Histamine H3

scholarly journals Increased Hypothalamic Signal Transducer and Activator of Transcription 3 Phosphorylation after Hindbrain Leptin Injection

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1509-1519 ◽  
Author(s):  
Marieke Ruiter ◽  
Patricia Duffy ◽  
Steven Simasko ◽  
Robert C. Ritter
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Fourth Ventricle ◽  
Leptin Receptor ◽  
Janus Kinase ◽  
Signal Transducer ◽  
Solitary Tract ◽  
Stat3 Signaling ◽  
Stat3 Phosphorylation ◽  
Transcription 3

Reduction of food intake and body weight by leptin is attributed largely to its action in the hypothalamus. However, the signaling splice variant of the leptin receptor, LRb, also is expressed in the hindbrain, and leptin injections into the fourth cerebral ventricle or dorsal vagal complex are associated with reductions of feeding and body weight comparable to those induced by forebrain leptin administration. Although these observations suggest direct hindbrain action of leptin on feeding and body weight, the possibility that hindbrain leptin administration also activates the Janus kinase/signal transducer and activator of transcription 3 (STAT3) signaling in the hypothalamus has not been investigated. Confirming earlier work, we found that leptin produced comparable reductions of feeding and body weight when injected into the lateral ventricle or the fourth ventricle. We also found that lateral and fourth ventricle leptin injections produced comparable increases of STAT3 phosphorylation in both the hindbrain and the hypothalamus. Moreover, injection of 50 ng of leptin directly into the nucleus of the solitary tract also increased STAT3 phosphorylation in the hypothalamic arcuate and ventromedial nuclei. Increased hypothalamic STAT3 phosphorylation was not due to elevation of blood leptin concentrations and the pattern of STAT3 phosphorylation did not overlap distribution of the retrograde tracer, fluorogold, injected via the same cannula. Our observations indicate that even small leptin doses administered to the hindbrain can trigger leptin-related signaling in the forebrain, and raise the possibility that STAT3 phosphorylation in the hypothalamus may contribute to behavioral and metabolic changes observed after hindbrain leptin injections.

scholarly journals The unsilent majority–TRPV1 drives “spontaneous” transmission of unmyelinated primary afferents within cardiorespiratory NTS

2012 ◽  
Vol 303 (12) ◽  
pp. R1207-R1216 ◽  
Author(s):  
Michael C. Andresen ◽  
Mackenzie E. Hofmann ◽  
Jessica A. Fawley
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Visceral Afferents ◽  
Transient Receptor Potential Vanilloid ◽  
Control Mechanisms ◽  
Solitary Tract ◽  
Organ Systems ◽  
Asynchronous Release ◽  
Transient Receptor ◽  
Afferent Terminals

Cranial primary afferent sensory neurons figure importantly in homeostatic control of visceral organ systems. Of the two broad classes of visceral afferents, the role of unmyelinated or C-type class remains poorly understood. This review contrasts key aspects of peripheral discharge properties of C-fiber afferents and their glutamate transmission mechanisms within the solitary tract nucleus (NTS). During normal prevailing conditions, most information arrives at the NTS through myelinated A-type nerves. However, most of visceral afferent axons (75–90%) in NTS are unmyelinated, C-type axons. Centrally, C-type solitary tract (ST) afferent terminals have presynaptic transient receptor potential vanilloid type 1 (TRPV1) receptors. Capsaicin activation of TRPV1 blocks phasic or synchronous release of glutamate but facilitates release of glutamate from a separate pool of vesicles. This TRPV1-operated pool of vesicles is active at normal temperatures and is responsible for actively driving a 10-fold higher release of glutamate at TRPV1 compared with TRPV1− terminals even in the absence of afferent action potentials. This novel TRPV1 mechanism is responsible for an additional asynchronous release of glutamate that is not present in myelinated terminals. The NTS is rich with presynaptic G protein-coupled receptors, and the implications of TRPV1-operated glutamate offer unique targets for signaling in C-type sensory afferent terminals from neuropeptides, inflammatory mediators, lipid metabolites, cytokines, and cannabinoids. From a homeostatic view, this combination could have broad implications for integration in chronic pathological disturbances in which the numeric dominance of C-type endings and TRPV1 would broadly disturb multisystem control mechanisms.

Regional effect of naltrexone in the nucleus of the solitary tract in blockade of NPY-induced feeding

2000 ◽  
Vol 278 (2) ◽  
pp. R499-R503 ◽  
Author(s):  
C. M. Kotz ◽  
M. J. Glass ◽  
A. S. Levine ◽  
C. J. Billington
Keyword(s):  
Cerebrospinal Fluid ◽  
Food Intake ◽  
Paraventricular Nucleus ◽  
Opioid Receptors ◽  
The Other ◽  
Solitary Tract ◽  
Sprague Dawley ◽  
Regional Effect ◽  
Sprague Dawley Rats ◽  
Artificial Cerebrospinal Fluid

Naltrexone (NLTX) in the nucleus of the solitary tract (NTS) decreases feeding induced by neuropeptide Y (NPY) in the paraventricular nucleus (PVN). We sought to determine the NTS region most sensitive to NLTX blockade of PVN NPY-induced feeding. Male Sprague-Dawley rats were fitted with two cannulas; one in the PVN and one in a hindbrain region: caudal, medial, or rostral NTS or 1 mm outside the NTS. Animals received NLTX (0, 1, 3, 10, and 30 μg in 0.3 μl) into the hindbrain region just prior to PVN NPY (0.5 μg, 0.3 μl) or artificial cerebrospinal fluid (0.3 μl). Food intake was measured at 2 h following injection. PVN NPY stimulated feeding, and NLTX in the medial NTS significantly decreased NPY-induced feeding at 2 h, whereas administration of NLTX in the other hindbrain regions did not significantly influence PVN NPY induced feeding. These data suggest that opioid receptors in the medial NTS are most responsive to feeding signals originating in the PVN after NPY stimulation.

scholarly journals Effect of glycomacropeptide fractions on cholecystokinin and food intake

2010 ◽  
Vol 104 (2) ◽  
pp. 286-290 ◽  
Author(s):  
Jennifer B. Keogh ◽  
Brad W. Woonton ◽  
Cheryl M. Taylor ◽  
Filip Janakievski ◽  
Kirthi Desilva ◽  
...  
Keyword(s):  
Food Intake ◽  
Cheese Whey ◽  
Whey Protein Concentrate ◽  
Subjective Measures ◽  
Double Blind ◽  
Acetylneuraminic Acid ◽  
Significant Difference ◽  
Acute Study ◽  
The Given ◽  
Food Consumed

Glycomacropeptide (GMP) is the hydrophilic 64-amino acid C-terminal glycopeptide released into cheese whey when κ-casein is cleaved by chymosin. GMP exists as a mixture of different glycoforms due to the carbohydrates sialic acid (N-acetylneuraminic acid, NeuNAc), galactose (Gal), galactosamine and glucosamine attached by O-glycosidic linkages. GMP reportedly stimulates the release of cholecystokinin (CCK), which may promote satiety. The objectives of the present study were to manufacture three glycoforms of GMP, minimally glycosylated GMP (3·5 (sd 0·1) % NeuNAc and 1·5 (sd 0·1) % Gal), glycosylated GMP (12·0 (sd 0·3) % NeuNAc and 4·2 (sd 0·2) % Gal) and a GMP-depleted whey protein concentrate, and to assess the effects of these fractions relative to glucose on CCK, subjective measures of satiety and food intake. In a randomised double-blind acute study, twenty overweight/obese males (56·9 (sd 7·2) years, 97·4 (sd 8·1) kg, 31·5 (sd 3·0) kg/m2) were recruited to consume four 50 g preloads (two GMP preparations, GMP-depleted whey and glucose) containing 895 kJ. Blood samples and subjective measures of satiety were collected before and at 15, 30, 60, 90, 120 and 180 min after the consumption of preload, and CCK levels were measured. A lunchtime meal of hot food was provided from which subjects ate ad libitum until satisfied. Energy and nutrient intakes from the food consumed were calculated. There was no significant difference in CCK levels, subjective measures of satiety or food intake between treatments at the given preload level. These results suggest that the protein fractions at the dose employed do not influence satiety, CCK levels or energy intake at a subsequent meal.

C-fos protein expression in the nucleus of the solitary tract correlates with cholecystokinin dose injected and food intake in rats

1999 ◽  
Vol 846 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Tilman T Zittel ◽  
Jörg Glatzle ◽  
Martin E Kreis ◽  
M Starlinger ◽  
M Eichner ◽  
...  
Keyword(s):  
Food Intake ◽  
Protein Expression ◽  
Solitary Tract ◽  
Fos Protein

scholarly journals Isoflurane Differentially Modulates Inhibitory and Excitatory Synaptic Transmission to the Solitary Tract Nucleus

2008 ◽  
Vol 108 (4) ◽  
pp. 675-683 ◽  
Author(s):  
James H. Peters ◽  
Stuart J. McDougall ◽  
David Mendelowitz ◽  
Dennis R. Koop ◽  
Michael C. Andresen
Keyword(s):  
Nucleus Tractus Solitarius ◽  
Second Order ◽  
Visceral Afferents ◽  
Gas Chromatography Mass Spectrometry ◽  
Gamma Aminobutyric Acid ◽  
Solitary Tract ◽  
Excitatory Postsynaptic Currents ◽  
Inhibitory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Presynaptic Mechanisms

Background Isoflurane anesthesia produces cardiovascular and respiratory depression, although the specific mechanisms are not fully understood. Cranial visceral afferents, which innervate the heart and lungs, synapse centrally onto neurons within the medial portion of the nucleus tractus solitarius (NTS). Isoflurane modulation of afferent to NTS synaptic communication may underlie compromised cardiorespiratory reflex function. Methods Adult rat hindbrain slice preparations containing the solitary tract (ST) and NTS were used. Shocks to ST afferents evoked excitatory postsynaptic currents with low-variability (SEM <200 mus) latencies identifying neurons as second order. ST-evoked and miniature excitatory postsynaptic currents as well as miniature inhibitory postsynaptic currents were measured during isoflurane exposure. Perfusion bath samples were taken in each experiment to measure isoflurane concentrations by gas chromatography-mass spectrometry. Results Isoflurane dose-dependently increased the decay-time constant of miniature inhibitory postsynaptic currents. At greater than 300 mum isoflurane, the amplitude of miniature inhibitory postsynaptic currents was decreased, but the frequency of events remained unaffected, whereas at equivalent isoflurane concentrations, the frequency of miniature excitatory postsynaptic currents was decreased. ST-evoked excitatory postsynaptic current amplitudes decreased without altering event kinetics. Isoflurane at greater than 300 mum increased the latency to onset and rate of synaptic failures of ST-evoked excitatory postsynaptic currents. Conclusions In second-order NTS neurons, isoflurane enhances phasic inhibitory transmission via postsynaptic gamma-aminobutyric acid type A receptors while suppressing excitatory transmission through presynaptic mechanisms. These results suggest that isoflurane acts through multiple distinct mechanisms to inhibit neurotransmission within the NTS, which would underlie suppression of homeostatic reflexes.

scholarly journals Electroacupuncture Alleviates Cisplatin-Induced Nausea in Rats

2016 ◽  
Vol 34 (2) ◽  
pp. 120-126 ◽  
Author(s):  
Yingxue Cui ◽  
Linpeng Wang ◽  
Guangxia Shi ◽  
Lu Liu ◽  
Pei Pei ◽  
...  
Keyword(s):  
High Performance Liquid Chromatography ◽  
Liquid Chromatography ◽  
Food Intake ◽  
Rat Model ◽  
High Performance ◽  
Mechanisms Of Action ◽  
Nausea And Vomiting ◽  
Solitary Tract ◽  
Beneficial Effects ◽  
Fos Expression

Objective Acupuncture has been shown to be effective for the treatment of chemotherapy-related nausea and vomiting. The aim of this study was to explore the mechanisms of action underlying the anti-emetic effect of electroacupuncture (EA). Design Forty-eight rats received saline (n=12) or 6 mg/kg cisplatin (n=36) to establish a chemotherapy-induced nausea and vomiting model. EA was performed at CV12 (n=12), bilateral PC6 (n=12), or sham points (n=12) 3 days before and 1–2 days after cisplatin administration (4–5 times in total), at 0.5–1 mA intensity and 2/15 Hz frequency for 10 min. Kaolin intake, food intake and bodyweight change were evaluated as markers of nausea and vomiting severity. Concentrations of serotonin (5-hydroxytryptamine, 5-HT) in the duodenum and c-Fos expression in the nucleus of the solitary tract (NTS) were measured using high performance liquid chromatography and immunohistochemistry, respectively. Results Cisplatin administration led to increased kaolin intake and reduced food intake and bodyweight over the following 2 days. EA at CV12 significantly reversed the cisplatin-induced change in kaolin intake (on days 1 and 2) and food intake and bodyweight (on day 1). EA at CV12 also attenuated the cisplatin-induced increase in 5-HT in the duodenum and suppressed c-Fos expression in the NTS. EA at PC6 influenced kaolin intake (on day 1 only) and c-Fos expression, but had no statistically significant effect on food intake, bodyweight or 5-HT expression. Conclusions This study demonstrated beneficial effects of EA on chemotherapy-induced nausea and vomiting in a rat model. The anti-emetic effect of EA may be mediated through inhibition of 5-HT secretion in the duodenum and activity of the NTS.

Estimating Food Intake by Captive Emus, Dromaius Novaehollandiae, by Means of Sodium-22 Turnover.

1985 ◽  
Vol 12 (3) ◽  
pp. 455 ◽  
Author(s):  
RM Herd
Keyword(s):  
Food Intake ◽  
Food Consumption ◽  
Reliable Method ◽  
Metabolizable Energy ◽  
Dietary Sodium ◽  
Free Living ◽  
Dromaius Novaehollandiae ◽  
Close Relationship ◽  
Gross Energy ◽  
Food Consumed

The rate of 22Na turnover was measured in 4 captive emus each fed on 3 diets. There was a close relationship between 22Na turnover and the intake of dietary sodium (r = 0.92), DM (r = 0.93), gross energy and metabolizable energy (r = 0.94). DM intake, estimated from 22Na turnover, accounted for 89% of the variation in actual DM intake, and suggested that 22Na turnover could provide a reliable method for estimating food consumption by populations of free-living emus. However, estimates of food consumed by individual animals may not be reliable.

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