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1 Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260; 2 Department of Medicine, Georgetown University, Washington, District of Columbia 20007; and 3 Department of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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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.
feeding behavior; gastric distension; catecholamines; nucleus of the solitary tract
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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GASTRIC DISTENSION PLAYS an important physiological role in promoting satiety to food ingestion (13, 26). Mechanical distension of the stomach in rats activates vagal mechanoreceptors with excitatory synaptic inputs to gastric sensory subregions of the dorsal vagal complex, comprising the nucleus of the solitary tract (NST), area postrema (AP), and dorsal motor nucleus of the vagus (DMV) (5, 14). Gastric distension signals are relayed from the NST to other areas of the hindbrain and forebrain that are involved in the control of feeding behavior.
Hindbrain neurons that are activated by gastric distension have been localized through immunocytochemical analysis of the immediate-early gene product c-Fos, which accumulates in neuronal nuclei subsequent to synaptic stimulation (9, 17). Neurons in similar subregions of the NST are activated to express c-Fos in rats after gastric balloon distension (2, 25) or after food ingestion (1, 2, 10), evidence that gastric distension produced by a meal contributes to NST activation. Conversely, neurons in the AP are not activated after gastric balloon distension alone (2, 25) but are activated after ingestion of a large meal (1, 2, 10). The aim of the present study was to determine whether c-Fos expression in the dorsal vagal complex and other hindbrain regions is quantitatively related to the magnitude of feeding-induced gastric distension. For this purpose, we examined the distribution and chemical phenotypes of hindbrain neurons activated to express c-Fos in rats after ingestion of a large satiating meal of pelleted chow or liquid diet, after ingestion of a smaller rationed meal of liquid diet, or after no meal.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Animals
Twenty-three male Sprague-Dawley rats (Zivic Miller, Zelienople, PA) weighing 300-350 g were used for these studies. Rats were housed singly in stainless steel wire mesh cages in a temperature-controlled room (20-22°C) with lights on from 0700 to 1900.Procedure
Feeding schedule. All rats were acclimated to a feeding schedule for 5 days, during which time water always was available. Rats had access to pelleted rodent chow (no. 5001; 3.0 kcal/g; Purina) for 3 h each afternoon and had access to either pelleted chow or liquid diet for 1 h each morning. The standard liquid diet consisted of 316 g of AIN-76 liquid diet powder (Bioserv) blended with 1 liter of 14% dextrose (Fisher Scientific) to yield a formula containing 1.42 kcal/ml and 1.2 mosM/ml. Rats in each treatment group maintained or increased their body weights during the acclimation period.Experimental treatment. On the morning of the experiment (day 5 of the acclimation period), one group of rats received their usual 1-h access to an unrestricted amount of pelleted chow (UC rats; n = 5). A second group of rats received their usual 1-h access to an unrestricted amount of standard liquid diet (stULD rats; n = 4). A third group of rats was given 1-h access to an unrestricted amount of liquid diet that had been diluted 50% with water to yield a solution containing 0.71 kcal/ml and 0.6 mosM/ml (dilULD rats; n = 4). A fourth group of rats received a rationed amount (10 ml) of standard liquid diet to consume during the 1-h feeding period (stRLD rats; n = 6). Their 10-ml ration was about one-third the volume consumed in 1 h by rats with free access to dilute liquid diet (see RESULTS). A fifth group of rats received no meal during the 1-h feeding period (unfed rats; n = 4).
Perfusion fixation. Thirty minutes after the end of the 1-h feeding period (between 1030 and 1130), rats were anesthetized with pentobarbital sodium (80 mg/kg ip) and killed by transcardiac perfusion fixation. Perfusates consisted of 100 ml of 0.15 M NaCl followed by 250 ml of 0.1 M potassium phosphate buffer (KPB) containing 4% paraformaldehyde with lysine and sodium metaperiodate (adapted from Ref. 8). The postmortem weight of gastric contents was recorded in each rat as an indirect measure of meal-induced gastric distension. Brains were postfixed for 2 h and then immersed for 24-48 h in aqueous 25% sucrose solution (4°C) before sectioning.
Tissue preparation and
immunocytochemistry. Brain stems were cut at 35 µm on
a freezing-stage microtome. Sections were collected in serially ordered
sets through the rostrocaudal extent of the DMV, so that each set
contained a 1:6 series of hindbrain sections spaced by 210 µm. Tissue
sections were stored at 
20°C in cryoprotectant (24). Before
immunocytochemical procedures, sections were removed from
cryoprotectant and rinsed in KPB. The anti-c-Fos serum used in the
present work was generated in rabbit against amino acids 4
17 of c-Fos
protein [Oncogene Science; the lot used (#40890207) is no longer
available commercially]. This antiserum does not recognize other
immediate-early gene products or Fos-related antigens (3). Antisera
were diluted in KPB containing 0.3% Triton X-100. Tissue sections were
incubated for 48 h at 4°C in anti-c-Fos (1:40,000), rinsed, and
then incubated in biotinylated goat anti-rabbit IgG (Jackson
ImmunoResearch; 1:600) for 1 h at room temperature. Sections were
treated with Elite Vectastain reagents (Vector) as described previously
(3). Diaminobenzidine (DAB) intensified with nickel sulfate was used to
produce a blue-black nuclear c-Fos reaction product.
One set of c-Fos-labeled hindbrain sections from each rat was processed
for immunoperoxidase localization of tyrosine hydroxylase (TH) to
identify catecholaminergic cells. Sections were incubated at 4°C
for 48 h in monoclonal anti-TH (Chemicon; 1:100,000), then were
processed as above using biotinylated goat anti-mouse IgG (Jackson
ImmunoResearch; 1:600) and Elite Vectastain reagents. DAB was used to
produce a brown cytoplasmic TH reaction product. This set of sections
was used for quantitative analysis of c-Fos expression by
catecholaminergic neurons (see below). A second set of hindbrain
sections was processed for immunofluorescent localization of dopamine
-hydroxylase (DBH) to allow black and white photographic
documentation of c-Fos expression by adrenergic and noradrenergic
neurons. For this purpose, sections were incubated at 4°C for 48 h
in mouse anti-DBH (Chemicon; 1:3,000), rinsed, incubated for 2 h at
room temperature in Cy3-conjugated
F(ab')2 fragment donkey
anti-mouse IgG (Jackson ImmunoResearch; 1:500), and rinsed thoroughly.
After immunocytochemical staining, tissue sections were mounted out of
KPB onto gelatin-coated microscope slides, dehydrated and defatted in
graded ethanols and Histoclear (VWR Scientific), and
placed under a coverslip with Histomount (VWR Scientific).
Data plotting and quantitative analysis. A custom computerized x-y coordinate plotting system was used to map immunolabeled cells from each rat in hindbrain tissue sections reacted for c-Fos and TH. As described above, these sections were spaced ~210 µm apart. Maps were made of tissue sections beginning at the most caudal level of the AP and extending through the most rostral level of the DMV (~8 tissue sections per rat). Tissue and nuclear boundaries were outlined using a ×10 microscope objective. Then, using a ×20 objective, the location of each c-Fos-positive and/or TH-positive cell was plotted. Cells were considered c-Fos-positive if they contained visible blue-black nuclear immunoreactivity. TH-positive cells were identified by the presence of brown cytoplasmic immunoreactivity and were plotted only when they displayed a visible nucleus. TH-positive cells were considered c-Fos-positive when their nucleus contained blue-black nuclear immunoreactivity, regardless of intensity, and were considered c-Fos-negative when they displayed a visible nucleus lacking blue-black immunoreactivity. The total number of catecholaminergic (TH positive) neurons in the NST and VLM and the percentage that were activated to express c-Fos were calculated for individual rats in each treatment group.
Statistical analysis. Data are presented as means ± SE. Statistical differences were determined using one-way analysis of variance across groups followed by Bonferroni comparisons between pairs of groups. Differences were considered statistically significant when P < 0.05.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Meal Size and Postmortem Gastric Contents
Unfed rats. Postmortem weight of gastric contents in unfed rats (n = 4) averaged 0.1 ± 0.1 g.Rationed liquid diet. stRLD rats
(n = 6) consumed their full 10-ml
ration of standard liquid diet (14.2 kcal and 12 mosM) during the 1-h
feeding period. Their gastric contents at death weighed 8.4 ± 0.6 g. Although rats consuming rationed or unrestricted amounts of liquid
diet (see below) had continual free access to water, no water was
ingested by stRLD rats during the 1-h feeding period. A few rats drank
1.0 ml of water during the 30-min survival time thereafter.
Unrestricted liquid diet. All ULD rats
(n = 8) stopped consuming liquid diet
before the end of the 1-h feeding period. stULD rats
(n = 4) consumed 25.2 ± 0.8 ml
(~35.8 kcal and 30.2 mosM). Their gastric contents at death weighed
20.6 ± 2.1 g. dilULD rats (n = 4)
consumed 30.5 ± 0.2 ml (~21.7 kcal and 18.3 mosM). Their gastric
contents at death weighed 25.8 ± 1.5 g. As with stRLD rats, ULD
rats drank no water during the 1-h feeding period, and only a few drank
1.0 ml of water during the 30-min survival time thereafter.
Unrestricted chow. Similar to ULD rats, all UC rats (n = 5) stopped eating before the end of the 1-h feeding period, during which time they consumed 10.6 ± 1.3 g of pelleted chow (~31.8 kcal; undetermined mosM). UC rats additionally drank 8.0 ± 0.5 ml of water during the 1-h feeding period but only 0.8 ± 0.5 ml during the 30-min survival time thereafter. Postmortem weight of gastric contents in UC rats averaged 16.3 ± 1.7 g.
Hindbrain c-Fos Expression
Very little c-Fos expression was observed within the AP, NST, VLM, or other hindbrain regions in unfed rats. Similarly, c-Fos was essentially absent from the AP and VLM in stRLD rats (Fig. 1A). Qualitative impressions suggested that the NST contained somewhat more c-Fos labeling in stRLD rats (Fig. 1A) compared with unfed rats. However, quantitative examination of catecholaminergic activation revealed no statistical difference between stRLD rats and unfed rats: very few TH-positive neurons in either the NST (Fig. 2A) or VLM (Fig. 2B) expressed c-Fos in either group.
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In contrast to the relatively low levels of hindbrain c-Fos expression in unfed rats and stRLD rats, large satiating meals of either pelleted chow (UC rats) or liquid diet (ULD rats) induced pronounced c-Fos expression within the medial NST and AP (Fig. 1B). Few or no DMV motoneurons expressed c-Fos in UC or ULD rats. Activated neurons in the dorsal vagal complex included TH-positive NST cells, primarily at caudal levels corresponding to the location of the A2 catecholamine cell group (Fig. 3, A and A*). Quantitative analysis demonstrated that similar proportions of TH-positive NST neurons expressed c-Fos in UC rats and in stULD rats (Fig. 2A), whereas significantly more TH-positive cells were activated in dilULD rats (P < 0.05 for each comparison; Fig. 2A). Catecholaminergic neurons in the VLM rarely expressed c-Fos in UC or ULD rats (Fig. 1B and Fig. 3, B and B*), similar to their lack of significant activation in unfed rats or stRLD rats (Fig. 2B).
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Correlation Between Postmortem Weight of Gastric Contents and Activation of Catecholaminergic NST Neurons
There was a significant positive correlation between the postmortem weight of gastric contents and the percent activation of catecholaminergic NST neurons in individual rats from the stRLD, ULD, and UC groups (Pearson r = 0.81; P < 0.0001; Fig. 4). Conversely, catecholaminergic NST activation was not significantly correlated with the number of calories or osmoles consumed by individual rats; in fact, the highest NST catecholaminergic activation values were measured in dilULD rats (Fig. 4). These rats consumed fewer calories and osmoles than UC or stULD rats, but achieved the largest gastric volumes as indicated by postmortem weight of gastric contents.
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Feeding involves numerous anticipatory, ingestive, and digestive processes, any of which might be expected to stimulate neurons in hindbrain circuits that control and/or are influenced by these processes. The present data suggest that such stimuli are insufficient to generate significant hindbrain c-Fos expression in freely feeding rats unless a satiating amount of liquid or solid food is consumed.
Relatively small amounts of gastric distension (e.g., as produced by intragastric infusion of 2.5 ml of saline) are sufficient to increase the firing activity of individual gastric vagal mechanoreceptors (19, 20) and to exert inhibitory control over subsequent food intake (13). In the present study, however, c-Fos expression in stRLD rats that consumed 10 ml of liquid diet (and had postmortem gastric contents weighing ~8.4 g) was not significantly different from c-Fos expression in unfed rats. These findings are consistent with evidence that stimulation thresholds for neuronal c-Fos expression are generally higher than stimulation thresholds for physiological or behavioral markers of neural activation (3, 9, 17). Such limitations notwithstanding, the present data demonstrate that a "dose-response" relationship can be described between feeding-induced gastric distension and activation of c-Fos expression in catecholaminergic NST neurons. On reaching satiety, ULD rats had consumed ~25.2 ml of standard liquid diet or 30.5 ml of diluted liquid diet, and UC rats had consumed ~10.6 g of chow and 8.0 ml of water. As shown in Fig. 4, the percentage of catecholaminergic NST neurons expressing c-Fos in individual rats across all fed groups was directly proportional to the weight of their gastric contents measured postmortem; conversely, catecholaminergic NST activation was not significantly related to the number of calories or osmoles consumed by individual rats during their final meal. These results suggest that a preabsorptive, gastric volume-related signal was largely responsible for the observed c-Fos activation. One interpretation of these data is that increasing amounts of feeding-induced gastric distension generated increasing amounts of vagal afferent stimulation, thereby increasing c-Fos expression in postsynaptic gastric mechanoreceptive NST neurons.
Electrophysiological data support a direct and proportional relationship between gastric distension and vagal mechanoreceptor activation: increasing distension is accompanied by increased firing rates of individual vagal mechanoreceptive units and progressive recruitment of additional units (19, 20). Electrophysiological studies also have shown that NST neurons receiving synaptic input from gastric vagal mechanoreceptors are almost invariably excited by gastric distension, whereas most distension-sensitive DMV motoneurons are concurrently inhibited (5). The present data reveal a similar pattern of neuronal c-Fos expression in satiated rats, consistent with the hypothesis that gastric distension played a principal role in the observed neuronal activation. Another recent study using the c-Fos technique showed that gastric balloon distension activates NST neurons, including catecholaminergic neurons, and that this activation is proportional to the degree of induced gastric distension (25). Although catecholaminergic neurons make up only a small proportion of the NST neurons activated to express c-Fos in rats after ingestion of a satiating meal (present data) or after gastric balloon distension (25), these neurons constitute the major direct ascending pathway through which vagal sensory information reaches autonomic, behavioral, and neuroendocrine centers in the hypothalamus and other forebrain areas (11, 15, 18).
The AP also contained many c-Fos-positive cells in rats after satiating meals of chow or liquid diet. It is of interest that rats with AP lesions consume normal daily amounts of food but in ingestive bouts that are much larger than those of intact rats, suggesting that the AP is important for detecting early inhibitory signals generated by food ingestion (21). Visceral sensory fibers that potentially are stimulated after ingestion of a large meal comprise not only distension-sensitive mechanoreceptors but also a variety of chemoreceptors sensitive to water, temperature, pH, hormones, and specific nutrients. Regarding the latter, duodenal infusions of certain macronutrients trigger c-Fos expression in both the AP and NST (12, 27). Conversely, gastric balloon distension by itself does not activate c-Fos expression in the AP, despite significant distension-induced NST activation (25). These and the present findings support the idea that a combination of distension- and nutrient-related signals contributes to NST and AP c-Fos expression in rats after ingestion of a large satiating meal, whereas such signals are below threshold for NST and AP c-Fos activation in rats after ingestion of a smaller rationed meal.
In considering other types of stimuli that might have contributed to hindbrain neuronal c-Fos expression in satiated rats but not in rats that ate a rationed meal, potential meal-induced changes in plasma volume and/or plasma osmolality seem relevant. If such changes were of significant magnitude to induce hindbrain c-Fos expression, they would also be expected to stimulate water drinking. Rats consuming pelleted chow did drink a significant amount of water during their meal (prandial drinking), and the factors that induced this drinking conceivably contributed to hindbrain c-Fos expression in those rats. However, hindbrain c-Fos expression in chow-fed rats was similar to that observed in liquid diet-fed rats, even though rats consuming liquid diet drank essentially no water either during their meal or in the 30-min survival time thereafter. Additional experiments will be required to differentiate among potential mechanical and chemoreceptive stimuli that may contribute to medullary c-Fos expression in rats after a satiating meal.
In summary, the present findings offer new supportive evidence for a direct, proportional relationship between meal-induced stimulation of distension-sensitive gastric vagal afferents and activation of catecholaminergic NST neurons. This relationship does not extend to catecholaminergic neurons in the VLM, which were not activated to express c-Fos even in rats that consumed a very large satiating meal. We conclude that catecholaminergic NST neurons may be activated in common by stimuli that excite gastric vagal mechanoreceptors and lead to cessation of feeding behavior (e.g., gastric balloon distension and ingestion of a large meal), whereas AP neurons and catecholaminergic VLM neurons are activated in a treatment-specific manner.
Perspectives
Meal-induced c-Fos expression in the rat hindbrain does not depend on endogenously released cholecystokinin (CCK) (1). However, systemic administration of CCK stimulates distension-sensitive gastric vagal afferents (19, 20) and produces distension-like effects on the firing activity of neurons in the dorsal vagal complex (14). Exogenous CCK also induces c-Fos expression in the NST and AP but not in the DMV (4, 10, 16), similar to the present results in rats that consumed a large satiating meal.CCK administered systemically at a dose of 10 µg/kg inhibits gastric emptying and feeding by ~80% (6, 7) and induces c-Fos expression in ~37% of catecholaminergic NST neurons (23). According to the regression line in Fig. 4, this amount of catecholaminergic NST activation corresponds to a hypothetical gastric volume of ~25 g, comparable to the highest values measured in satiated rats in the present study. Thus a 10 µg/kg dose of CCK may produce stimulation of distension-sensitive gastric vagal afferents equivalent to that provided by consumption of a very large meal. It is of interest that an even higher dose of CCK (100 µg/kg) activates ~51% of catecholaminergic NST neurons (16) and eliminates feeding entirely (7). Such quantitative relationships offer supportive evidence for a direct and proportional linkage between physiological or pharmacological stimulation of gastric vagal mechanoreceptor inputs to catecholaminergic NST neurons and concomitant inhibition of feeding behavior.
Despite similarities between meal- and CCK-induced c-Fos expression in the dorsal vagal complex, a striking treatment-related difference was noted in the VLM. c-Fos expression was essentially absent from catecholaminergic VLM neurons in satiated UC and ULD rats, despite marked NST activation apparent in the same tissue sections. This finding stands in contrast to previous results demonstrating that a 100 µg/kg dose of CCK activates ~25% of catecholaminergic VLM neurons (primarily A1 cells) (16). We also have found that a 10-fold lower dose of CCK activates a similar proportion of catecholaminergic VLM neurons (21%; unpublished results). Previous reports of hindbrain c-Fos expression in rats after gastric balloon distension (2, 25) or after food ingestion (1, 2, 10) have not commented on the presence or absence of activated VLM neurons. We speculate that CCK-induced activation of catecholaminergic VLM neurons is due to stimulation of excitatory inputs to the VLM that are not stimulated after ingestion of even a very large meal. Alternatively, some aspect of feeding or its postingestive consequences may create neural signals that inhibit VLM neurons. Further work is needed to address this issue.
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ACKNOWLEDGEMENTS |
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This work was funded by National Institutes of Health Grants MH-01208, NS-28477, and MH-25140.
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FOOTNOTES |
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Portions of this study were presented at the 25th Annual Meeting of the Society for Neuroscience (Ref. 23).
Present address of G.E. Hoffman: Dept. of Anatomy, University of Maryland School of Medicine, Baltimore, MD 21201.
Address for reprint requests: L. Rinaman, Dept. of Neuroscience, Univ. of Pittsburgh, 446 Crawford Hall, Pittsburgh, PA 15260.
Received 8 July 1997; accepted in final form 31 March 1998.
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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  T. Babic, R. L. Townsend, L. M. Patterson, G. M. Sutton, H. Zheng, and H.-R. Berthoud Phenotype of neurons in the nucleus of the solitary tract that express CCK-induced activation of the ERK signaling pathway Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2009; 296(4): R845 - R854. [Abstract] [Full Text] [PDF]
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M. Fry and A. V. Ferguson Ghrelin modulates electrical activity of area postrema neurons Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2009; 296(3): R485 - R492. [Abstract] [Full Text] [PDF]
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 E. T. Uchoa, H. A. C. Sabino, S. G. Ruginsk, J. Antunes-Rodrigues, and L. L. K. Elias Hypophagia induced by glucocorticoid deficiency is associated with an increased activation of satiety-related responses J Appl Physiol, February 1, 2009; 106(2): 596 - 604. [Abstract] [Full Text] [PDF]
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C. M. Kotz, M. A. Mullett, and C. Wang Diminished feeding responsiveness to orexin A (hypocretin 1) in aged rats is accompanied by decreased neuronal activation Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2005; 289(2): R359 - R366. [Abstract] [Full Text] [PDF]
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H. Zheng, L. M. Patterson, C. B. Phifer, and H.-R. Berthoud Brain stem melanocortinergic modulation of meal size and identification of hypothalamic POMC projections Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2005; 289(1): R247 - R258. [Abstract] [Full Text] [PDF]
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L. A. Eckel, T. A. Houpt, and N. Geary Estradiol treatment increases CCK-induced c-Fos expression in the brains of ovariectomized rats Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2002; 283(6): R1378 - R1385. [Abstract] [Full Text] [PDF]
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L. A. Eckel and N. Geary Estradiol treatment increases feeding-induced c-Fos expression in the brains of ovariectomized rats Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2001; 281(3): R738 - R746. [Abstract] [Full Text] [PDF]
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M. Emond, G. J. Schwartz, and T. H. Moran Meal-related stimuli differentially induce c-Fos activation in the nucleus of the solitary tract Am J Physiol Regulatory Integrative Comp Physiol, May 1, 2001; 280(5): R1315 - R1321. [Abstract] [Full Text] [PDF]
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 J. J. Guo, K. N. Browning, R. C. Rogers, and R. A. Travagli Catecholaminergic neurons in rat dorsal motor nucleus of vagus project selectively to gastric corpus Am J Physiol Gastrointest Liver Physiol, March 1, 2001; 280(3): G361 - G367. [Abstract] [Full Text] [PDF]
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H. Yang, K. Kawakubo, H. Wong, G. Ohning, J. Walsh, and Y. Tache Peripheral PYY inhibits intracisternal TRH-induced gastric acid secretion by acting in the brain Am J Physiol Gastrointest Liver Physiol, September 1, 2000; 279(3): G575 - G581. [Abstract] [Full Text] [PDF]
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H. H. Bae, J. L. Stamper, E. C. Heydorn, I. Zucker, and J. Dark Role of area postrema in control of torpor in Siberian hamsters Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2000; 279(2): R591 - R598. [Abstract] [Full Text] [PDF]
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M. Covasa, R. C. Ritter, and G. A. Burns Reduction of food intake by intestinal macronutrient infusion is not reversed by NMDA receptor blockade Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2000; 278(2): R345 - R351. [Abstract] [Full Text] [PDF]
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L. Rinaman Interoceptive stress activates glucagon-like peptide-1 neurons that project to the hypothalamus Am J Physiol Regulatory Integrative Comp Physiol, August 1, 1999; 277(2): R582 - R590. [Abstract] [Full Text] [PDF]
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, Catecholaminergic (TH positive) neurons that do not express
c-Fos; 
, c-Fos-positive catecholaminergic neurons. AMB, nucleus
ambiguus; CC, central canal; CU, cuneate nucleus; GR, gracile nucleus;
Hyp, hypoglossal nucleus; IO, inferior olive; LRNm, LRNp, lateral
reticular nucleus (magnocellular, parvocellular); ml, medial lemniscus;
mlf, medial longitudinal fasciculus; co, commissural subnucleus of the
NST; ge, subnucleus gelatinosus of the NST; lat, lateral subnucleus of
the NST; m, medial subnucleus of the NST; sptV, spinal trigeminal
tract; ts, tractus solitarius; py, pyramidal tract. Scale bar = 0.5 mm.
