Duodenal nutrient infusions differentially affect sham feeding and Fos expression in rat brain stem

1998 ◽  
Vol 274 (6) ◽  
pp. R1725-R1733 ◽  
Author(s):  
Curtis B. Phifer ◽  
Hans-Rudolf Berthoud
Keyword(s):  
Amino Acids ◽  
Linoleic Acid ◽  
Area Postrema ◽  
Gastric Distension ◽  
Acid Mixture ◽  
Neural Pathways ◽  
Solitary Tract ◽  
Sham Feeding ◽  
Caloric Value ◽  
Fos Expression

Duodenal infusions of macronutrients inhibit sham and normal feeding. Neural substrates of this response were studied by infusing glucose, linoleic acid, an amino acid mixture, saline, or water into the duodenum of unanesthetized rats and then measuring sham feeding of 30% sucrose or Fos expression in the dorsal vagal complex. Linoleic acid and amino acids (both 1.5 kcal) and glucose (4.5 kcal) suppressed sham feeding relative to control infusions, and all three macronutrients triggered Fos expression in the nucleus of the solitary tract and area postrema. Although there were significant quantitative differences, the subnuclear distribution pattern of Fos-expressing neurons was not different for the three macronutrients and was largely localized to the medial, dorsomedial, and commissural subnuclei of the nucleus of the solitary tract and the area postrema. Linoleic acid suppressed intake and stimulated Fos expression similarly to glucose infusions of three times the caloric value. Amino acids strongly suppressed sham feeding but triggered relatively little Fos expression. These results indicate that the intake-suppressing potency of duodenal macronutrients is dependent on nutrient type, rather than simply caloric value, and that amino acids, although potent inducers of satiety, affect ingestion by processes different from those subserving lipids and carbohydrates. Furthermore, the similar patterns of neuronal activation after different duodenal infusions may indicate a large degree of convergence at the level of primary and second-order sensory neurons, whereas the distinctly different pattern obtained earlier with gastric distension indicates partially separate neural pathways for satiety signals generated by duodenal nutrients and gastric mechanoreceptors.

CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents

2005 ◽  
Vol 289 (3) ◽  
pp. R695-R703 ◽  
Author(s):  
E. H. E. M. van de Wall ◽  
P. Duffy ◽  
R. C. Ritter
Keyword(s):  
Vagal Afferents ◽  
Gastric Distension ◽  
Solitary Tract ◽  
C Fibers ◽  
Balloon Distension ◽  
Electrophysiological Responses ◽  
Vagal Afferent ◽  
Fos Expression ◽  
Afferent Response ◽  
And Control

Capsaicin treatment destroys vagal afferent C fibers and markedly attenuates reduction of food intake and induction of hindbrain Fos expression by CCK. However, both anatomical and electrophysiological data indicate that some gastric vagal afferents are not destroyed by capsaicin. Because CCK enhances behavioral and electrophysiological responses to gastric distension in rats and people, we hypothesized that CCK might enhance the vagal afferent response to gastric distension via an action on capsaicin-insensitive vagal afferents. To test this hypothesis, we quantified expression of Fos-like immunoreactivity (Fos) in the dorsal vagal complex (DVC) of capsaicin-treated (Cap) and control rats (Veh), following gastric balloon distension alone and in combination with CCK injection. In Veh rats, intraperitoneal CCK significantly increased DVC Fos, especially in nucleus of the solitary tract (NTS), whereas in Cap rats, CCK did not significantly increase DVC Fos. In contrast to CCK, gastric distension did significantly increase Fos expression in the NTS of both Veh and Cap rats, although distension-induced Fos was attenuated in Cap rats. When CCK was administered during gastric distension, it significantly enhanced NTS Fos expression in response to distension in Cap rats. Furthermore, CCK's enhancement of distension-induced Fos in Cap rats was reversed by the selective CCK-A receptor antagonist lorglumide. We conclude that CCK directly activates capsaicin-sensitive C-type vagal afferents. However, in capsaicin-resistant A-type afferents, CCK's principal action may be facilitation of responses to gastric distension.

Effect of vagal and splanchnic nerve section on Fos expression in ferret brain stem after emetic stimuli

1996 ◽  
Vol 271 (1) ◽  
pp. R228-R236 ◽  
Author(s):  
F. M. Boissonade ◽  
J. S. Davison
Keyword(s):  
Vagus Nerve ◽  
Brain Stem ◽  
Area Postrema ◽  
Splanchnic Nerve ◽  
Vagal Afferents ◽  
Sham Operation ◽  
Relative Importance ◽  
Solitary Tract ◽  
Nerve Section ◽  
Fos Expression

Previous studies have demonstrated that intraduodenal hypertonic saline (IHS) induces dense Fos expression within two regions of the ferret dorsal vagal complex (DVC): the area postrema (AP) and the medial subnucleus of the nucleus of the solitary tract (mn). The aims of the present experiments were to determine the peripheral pathways involved in excitation of DVC neurons after IHS and the relative importance of mn and AP excitation in the emetic response to this stimulus. The emetic response and the distribution of Fos were examined after IHS in animals that had received either vagotomy alone, vagotomy and splanchnic nerve section, or sham operation. The emetic response was studied in both awake and anesthetized animals, and Fos induction was studied in anesthetized animals. Vagotomy alone or combined with splanchnic nerve section abolished the emetic response and the area of dense labeling within the mn and reduced but did not abolish the labeling in the AP. It was concluded that both the emetic reflex and the dense expression of Fos within the mn after IHS are dependent on an intact vagus nerve. The excitation of neurons in the AP after IHS is partially dependent on vagal afferents, and the residual labeling that is present in the AP of neurectomized animals may be mediated via a blood-borne route.

Vestibular-mediated increase in central serotonin plays an important role in hypergravity-induced hypophagia in rats

2010 ◽  
Vol 109 (6) ◽  
pp. 1635-1643 ◽  
Author(s):  
Chikara Abe ◽  
Kunihiko Tanaka ◽  
Chihiro Iwata ◽  
Hironobu Morita
Keyword(s):  
Area Postrema ◽  
Vestibular Nucleus ◽  
Central Nucleus ◽  
Medial Vestibular Nucleus ◽  
Hypothalamic Nucleus ◽  
Solitary Tract ◽  
Afferent Pathway ◽  
Vestibular Input ◽  
Paraventricular Hypothalamic Nucleus ◽  
Fos Expression

Exposure to a hypergravity environment induces acute transient hypophagia, which is partially restored by a vestibular lesion (VL), suggesting that the vestibular system is involved in the afferent pathway of hypergravity-induced hypophagia. When rats were placed in a 3-G environment for 14 days, Fos-containing cells increased in the paraventricular hypothalamic nucleus, the central nucleus of the amygdala, the medial vestibular nucleus, the raphe nucleus, the nucleus of the solitary tract, and the area postrema. The increase in Fos expression was completely abolished or significantly suppressed by VL. Therefore, these regions may be critical for the initiation and integration of hypophagia. Because the vestibular nucleus contains serotonergic neurons and because serotonin (5-HT) is a key neurotransmitter in hypophagia, with possible involvement in motion sickness, we hypothesized that central 5-HT increases during hypergravity and induces hypophagia. To examine this proposition, the 5-HT concentrations in the cerebrospinal fluid were measured when rats were reared in a 3-G environment for 14 days. The 5-HT concentrations increased in the hypergravity environment, and these increases were completely abolished in rats with VL. Furthermore, a 5-HT2A antagonist (ketanserin) significantly reduced 3-G (120 min) load-induced Fos expression in the medial vestibular nucleus, and chronically administered ketanserin ameliorated hypergravity-induced hypophagia. These results indicate that hypergravity induces an increase in central 5-HT via the vestibular input and that this increase plays a significant role in hypergravity-induced hypophagia. The 5-HT2A receptor is involved in the signal transduction of hypergravity stress in the vestibular nucleus.

scholarly journals Effect of brain stem NMDA-receptor blockade by MK-801 on behavioral and Fos responses to vagal satiety signals

1999 ◽  
Vol 277 (4) ◽  
pp. R1104-R1111 ◽  
Author(s):  
Huiyuan Zheng ◽  
Lisa Kelly ◽  
Laurel M. Patterson ◽  
Hans-Rudolf Berthoud
Keyword(s):  
Nmda Receptor ◽  
Area Postrema ◽  
Additive Model ◽  
Nmda Receptor Antagonist ◽  
Gastric Distension ◽  
Motor Nucleus ◽  
Sucrose Intake ◽  
Mk 801 ◽  
Dorsal Motor Nucleus ◽  
Fos Expression

To test the possible role of N-methyl-d-aspartate (NMDA) glutamate receptors in the transmission of gastrointestinal satiety signals at the level of the nucleus of the solitary tract (NTS), we assessed the effect of fourth ventricular infusion of the noncompetitive NMDA receptor antagonist MK-801 on short-term sucrose intake and on gastric distension-induced Fos expression in the dorsal vagal complex of unanesthetized rats. MK-801, although not affecting initial rate of intake, significantly increased sucrose intake during the later phase of the meal (10–30 min, 8.9 ± 1.0 vs. 2.9 ± 0.8 ml, P < 0.01). In the medial subnucleus of the NTS, the area postrema, and the dorsal motor nucleus, MK-801 did not reduce gastric distension-induced Fos expression and itself did not significantly induce Fos expression. In the dorsomedial, commissural, and gelatinosus subnuclei, MK-801 in itself produced significant Fos expression and significantly reduced (−75%, P < 0.05) the ability of gastric distension to induce Fos expression, assuming an additive model with two separate populations of neurons activated by distension and the blocker. Although these results are consistent with NMDA receptor-mediated glutamatergic transmission of vagal satiety signals in general, they lend limited support for such a role in the transmission of specific gastric distension signals.

Oral-pharyngeal-esophageal and gastric cues contribute to meal-induced c-fos expression

1995 ◽  
Vol 268 (1) ◽  
pp. R223-R230 ◽  
Author(s):  
K. A. Fraser ◽  
E. Raizada ◽  
J. S. Davison
Keyword(s):  
Area Postrema ◽  
Receptor Activation ◽  
Gastric Distension ◽  
Motor Nucleus ◽  
Gastric Fistula ◽  
Gastric Balloon ◽  
Sham Feeding ◽  
Dorsal Motor Nucleus ◽  
Caudal Level

We recently demonstrated that a meal induces c-fos immunoreactivity in the dorsal motor nucleus of the vagus (DMV), the nucleus of the tractus solitarius (NTS), and the area postrema (AP) of the rat brain stem. This response was not eliminated by the cholecystokinin A (CCK-A) antagonist L-364,718, a finding suggesting that feeding induces c-fos immunoreactivity by a pathway that is largely independent of CCK-A receptor activation. Consequently, the role of alternative gastrointestinal cues in the induction of c-fos was investigated. The induction of c-fos after oral-pharyngeal and esophageal stimuli was examined by use of a sham-feeding procedure via a gastric fistula. Gastric fistula-closed and fed rats displayed c-fos immunoreactivity similar to that of meal-fed rats seen previously. Fistula-open and fed rats showed the same degree of staining in the more rostral section of NTS examined as fistula-closed and fed rats, but fewer c-fos-positive nuclei in the more caudal level of the NTS. The potential for gastric distension to induce c-fos was assessed after the inflation of a gastric balloon. Physiological inflation of the balloon produced marked c-fos induction primarily in the medial NTS.

Medullary c-Fos activation in rats after ingestion of a satiating meal

1998 ◽  
Vol 275 (1) ◽  
pp. R262-R268 ◽  
Author(s):  
L. Rinaman ◽  
E. A. Baker ◽  
G. E. Hoffman ◽  
E. M. Stricker ◽  
J. G. Verbalis
Keyword(s):  
Area Postrema ◽  
Vagal Afferents ◽  
Early Gene ◽  
Ventrolateral Medulla ◽  
Gastric Distension ◽  
Neural Activation ◽  
Food Ingestion ◽  
Catecholaminergic Neurons ◽  
Medial Nucleus ◽  
Fos Expression

The distribution and chemical phenotypes of hindbrain neurons that are activated in rats after food ingestion were examined. Rats were anesthetized and perfused with fixative 30 min after the end of 1-h meals of an unrestricted or rationed amount of food, or after no meal. Brain sections were processed for localization of the immediate-early gene product c-Fos, a marker of stimulus-induced neural activation. Hindbrain c-Fos expression was low in rats that ate a rationed meal or no meal. Conversely, c-Fos was prominent in the medial nucleus of the solitary tract (NST) and area postrema in rats that ate to satiety. There was a significant positive correlation between postmortem weight of gastric contents and the proportion of NST catecholaminergic neurons expressing c-Fos. Cells in the ventrolateral medulla (VLM) were not activated in rats after food ingestion, in contrast with previous findings that stimulation of gastric vagal afferents with anorexigenic doses of cholecystokinin activates c-Fos expression in both NST and VLM catecholaminergic cells. These findings indicate that anatomically distinct subsets of hindbrain catecholaminergic neurons are activated in rats after food ingestion and that activation of these cells is quantitatively related to the magnitude of feeding-induced gastric distension.

Area postrema lesions: cause of overingestion is not altered visceral nerve function

1986 ◽  
Vol 251 (3) ◽  
pp. R575-R581 ◽  
Author(s):  
G. L. Edwards ◽  
R. C. Ritter
Keyword(s):  
Motor Neurons ◽  
Area Postrema ◽  
Sucrose Solution ◽  
Solitary Tract ◽  
Palatable Food ◽  
Previous Suggestion ◽  
Sham Feeding ◽  
Efferent Function ◽  
Vagal Function ◽  
Intact Rats

Rats with lesions of the area postrema and the immediately subjacent nucleus of the solitary tract (AP lesions) ingest greater quantities of palatable foods than intact rats. Because AP lesions destroy some abdominal vagal sensory terminals and may damage vagal motor neurons as well, it is possible that lesion-induced alteration of vagal function causes overingestion of palatable foods. To test this hypothesis, we have examined ingestion of a highly palatable solid food by AP- and sham-lesioned rats with total subdiaphragmatic vagotomies and examined ingestion of a highly palatable sucrose solution by AP- and sham-lesioned rats with open gastric fistulas (sham feeding). Vagotomy in sham-lesioned rats failed to cause overingestion of palatable food. Furthermore, vagotomy in AP-lesioned rats did not abolish their overingestion of palatable food, although AP lesion-induced overingestion was attenuated by vagotomy. Finally, sham-feeding AP-lesioned rats consumed significantly more sucrose solution than sham-lesioned rats. These results indicate that overingestion of palatable foods and solutions by AP-lesioned rats is not due to impaired abdominal visceral afferent function and probably is not due to altered vagal efferent function. The data are consistent with our previous suggestion that overingestion by AP-lesioned rats results from a primary change in responsiveness to orosensory cues.

Gastric distension-induced release of 5-HT stimulates c-fos expression in specific brain nuclei via 5-HT3 receptors in conscious rats

2004 ◽  
Vol 287 (1) ◽  
pp. G228-G235 ◽  
Author(s):  
Takayuki Mazda ◽  
Hiroshi Yamamoto ◽  
Masaki Fujimura ◽  
Mineko Fujimiya
Keyword(s):  
Area Postrema ◽  
Gastric Wall ◽  
Afferent Nerve ◽  
Gastric Distension ◽  
Nerve Terminals ◽  
Afferent Pathways ◽  
Brain Nuclei ◽  
Ec Cells ◽  
Vagal Afferent ◽  
Fos Expression

We examined c- fos expression in specific brain nuclei in response to gastric distension and investigated whether 5-HT released from enterochromaffin (EC) cells was involved in this response. The role of 5-HT3 receptors in this mechanism was also addressed. Release of 5-HT was examined in an ex vivo-perfused stomach model, whereas c- fos expression in brain nuclei induced by gastric distension was examined in a freely moving conscious rat model. Physiological levels of gastric distension stimulated the vascular release of 5-HT more than luminal release of 5-HT, and induced c- fos expression in the nucleus of the solitary tract (NTS), area postrema (AP), paraventricular nucleus (PVN), and supraoptic nucleus (SON). The c- fos expression in all these brain nuclei was blocked by truncal vagotomy as well as by perivagal capsaicin treatment, suggesting that vagal afferent pathways may mediate this response. Intravenous injection of 5-HT3 receptor antagonist granisetron blocked c- fos expression in all brain nuclei examined, although intracerebroventricular injection of granisetron had no effect, suggesting that 5-HT released from the stomach may activate 5-HT3 receptors located in the peripheral vagal afferent nerve terminals and then induce brain c- fos expression. c- fos Positive cells in the NTS were labeled with retrograde tracer fluorogold injected in the PVN, suggesting that neurons in the NTS activated by gastric distension project axons to the PVN. The present results suggest that gastric distension stimulates 5-HT release from the EC cells and the released 5-HT may activate 5-HT3 receptors located on the vagal afferent nerve terminals in the gastric wall leading to neuron activation in the NTS and AP and subsequent activation of neurons in the PVN and SON.

Fos expression in ferret dorsal vagal complex after peripheral emetic stimuli

1994 ◽  
Vol 266 (4) ◽  
pp. R1118-R1126 ◽  
Author(s):  
F. M. Boissonade ◽  
K. A. Sharkey ◽  
J. S. Davison
Keyword(s):  
Electrical Stimulation ◽  
Hypertonic Saline ◽  
Area Postrema ◽  
Dorsal Vagal Complex ◽  
Solitary Tract ◽  
Communicating Branch ◽  
Nuclear Phosphoprotein ◽  
Fos Expression ◽  
Hypertonic Saline Injection ◽  
Stimulation Of

The aim of this study was to investigate neuronal activation in the dorsal vagal complex of the halothane-anesthetized ferret after peripheral emetic stimuli. Neuronal activity was studied by examining the distribution of the nuclear phosphoprotein Fos using immunohistochemistry. The emetic stimuli used were electrical stimulation of the supradiaphragmatic vagal communicating branch (SVCB) or intraduodenal injection of hypertonic saline. Electrical stimulation of the SVCB induced the densest Fos expression within the medial subnucleus of the nucleus of the solitary tract. After hypertonic saline injection, the greatest density of Fos-positive nuclei was observed within the area postrema and also in the medial subnucleus of the nucleus of the solitary tract. It was concluded that the emetic response to hypertonic saline involves neurons in both the area postrema and the nucleus of the solitary tract, especially the medial subnucleus, and that the medial subnucleus is important in the emetic response to SVCB stimulation.

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