Inhibition of food intake induced by acute stress in rats is due to satiation effects

Calvez, Juliane; Fromentin, Gilles; Nadkarni, Nachiket A.; Darcel, Nicolas; Even, Patrick C.; Tomé, Daniel; Ballet, Nathalie; Chaumontet, Catherine

doi:10.1016/j.physbeh.2011.07.012

Cited by 67 publications

(59 citation statements)

References 59 publications

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“…Previous work in rodents has shown that acute stress induces hypophagia [9], while food restriction can block the induction of responses to acute stress [10]. These findings, together with our observation that food-restricted mice avoided shocks much less frequently than fed mice (Figure S3A–B; p<0.001), led us to hypothesize that AgRP neuron activation may simultaneously suppress behavioral responses to threats while promoting food-seeking, perhaps as a means of prioritizing certain motivated behaviors over others [11].…”

Section: Resultsmentioning

confidence: 99%

Preemptive Stimulation of AgRP Neurons in Fed Mice Enables Conditioned Food Seeking under Threat

et al. 2016

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Summary The decision to engage in food-seeking behavior depends not only on homeostatic signals related to energy balance [1] but also on the presence of competing motivational drives [2] and learned cues signaling food availability [3]. Agouti-related peptide (AgRP) neurons in the arcuate nucleus of the hypothalamus (ARC) are critical for homeostatic feeding behavior. Selective ablation or silencing of AgRP neurons causes anorexia [4,6] while selective stimulation in fed mice promotes feeding and learned instrumental actions to obtain food rewards [5–8]. However, it remains unknown whether AgRP neuron stimulation is sufficient to drive food-seeking behavior in the continued presence of a competing motivational drive, such as threat avoidance, or whether it can drive discrimination between learned sensory cues associated with food rewards and other outcomes. Here, we trained mice to perform a sensory discrimination task involving appetitive and aversive visual cues. Food-restricted mice exhibited selective operant responding to food-predicting cues but largely failed to avoid cued shocks by moving onto a safety platform. The opposite was true following re-feeding. Strikingly, AgRP neuron photostimulation did not restore operant responding in fed mice when initiated within the threat-containing arena, but did when initiated in the home cage, prior to arena entry. These data suggest that the choice to pursue certain behaviors and not others (e.g. food seeking vs. shock avoidance) can depend on the temporal primacy of one motivational drive relative to the onset of a competing drive.

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Section: Resultsmentioning

confidence: 99%

Preemptive Stimulation of AgRP Neurons in Fed Mice Enables Conditioned Food Seeking under Threat

et al. 2016

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“…In rats, GLP-1 neurons are activated to express the immediate-early gene product cFos in response to experimental treatments that reduce meal size, including restraint stress (7), intraperitoneal injection of cholecystokinin (24,27,38), or gastric distension (8,36). A recent study in our laboratory explored whether food intake itself activates cFos expression by GLP-1 neurons (21).…”

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confidence: 99%

Hindbrain glucagon-like peptide-1 neurons track intake volume and contribute to injection stress-induced hypophagia in meal-entrained rats

Kreisler

Rinaman

2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Kreisler AD, Rinaman L. Hindbrain glucagon-like peptide-1 neurons track intake volume and contribute to injection stress-induced hypophagia in meal-entrained rats. Am J Physiol Regul Integr Comp Physiol 310: R906 -R916, 2016. First published March 2, 2016 doi:10.1152/ajpregu.00243.2015.-Published research supports a role for central glucagon-like peptide 1 (GLP-1) signaling in suppressing food intake in rodent species. However, it is unclear whether GLP-1 neurons track food intake and contribute to satiety, and/or whether GLP-1 signaling contributes to stress-induced hypophagia. To examine whether GLP-1 neurons track intake volume, rats were trained to consume liquid diet (LD) for 1 h daily until baseline intake stabilized. On test day, schedule-fed rats consumed unrestricted or limited volumes of LD or unrestricted volumes of diluted (calorically matched to LD) or undiluted Ensure. Rats were perfused after the test meal, and brains processed for immunolocalization of cFos and GLP-1. The large majority of GLP-1 neurons expressed cFos in rats that consumed satiating volumes, regardless of diet type, with GLP-1 activation proportional to intake volume. Since GLP-1 signaling may limit intake only when such large proportions of GLP-1 neurons are activated, a second experiment examined the effect of central GLP-1 receptor (R) antagonism on 2 h intake in schedule-fed rats. Compared with baseline, intracerebroventricular vehicle (saline) suppressed Ensure intake by ϳ11%. Conversely, intracerebroventricular injection of vehicle containing GLP-1R antagonist increased intake by ϳ14% compared with baseline, partly due to larger second meals. We conclude that GLP-1 neural activation effectively tracks liquid diet intake, that intracerebroventricular injection suppresses intake, and that central GLP-1 signaling contributes to this hypophagic effect. GLP-1 signaling also may contribute to satiety after large volumes have been consumed, but this potential role is difficult to separate from a role in the hypophagic response to intracerebroventricular injection.cFos; Exendin-3 (9 -39), Ex9; meal patterns FOOD INTAKE IS REGULATED BY a complex, neurochemically diverse neural network distributed within the brain stem, hypothalamus, and limbic forebrain. Food intake is the product of meal number (determined by signals that initiate feeding bouts) and meal size (determined by signals that terminate feeding bouts) (32). When rats in a controlled laboratory environment have unlimited access to standard chow, meal size is largely determined by feeding-generated satiety signals arising from the gastrointestinal (GI) tract that are delivered by vagal sensory inputs to the caudal nucleus of the solitary tract (cNST) (4, 12, 14 -18). The cNST relays satiety signals to a variety of central regions, including brain-stem pattern generator and premotor circuits that control the motoric components of feeding (i.e., licking, chewing, and swallowing) (31, 34). While it is clear that the cNST is critically involved in receiving and processing sig...

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“…The underlying mechanisms of acute stress-related reduction of food intake are largely linked to the activation of corticotropin releasing factor (CRF) signaling pathways. It is well documented that various stressors including wrap restraint stress, low dose of lipopolysaccharide, or abdominal surgery activate the hypothalamic/CRF-pituitary-adrenal axis as shown by Fos or Fos/CRF colabeling in stress-responsive hypothalamic regions and the related elevation of circulating adrenocorticotropic hormone (ACTH) and corticosterone (8,19). Moreover, CRF and the related peptides urocortin 1 or urocortin 2 injected centrally or peripherally reduce feeding via activation of brain CRF receptor subtypes 1 (CRF 1 ) and 2 (CRF 2 ) and peripheral CRF 2 receptor in rats (48,67,71).…”

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confidence: 99%

“…For instance, we previously reported that acute intraperitoneal (ip) injection of the immune stressor lipopolysaccharide at a low dose (100 g/kg) reduced the food intake response to a fast in rats (7). Similarly, a visceral stressor (abdominal surgery) or psychological stressors (restraint or novel environment) reduced the refeeding response to an overnight fast in rats (8,45,55). The underlying mechanisms of acute stress-related reduction of food intake are largely linked to the activation of corticotropin releasing factor (CRF) signaling pathways.…”

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confidence: 99%

Orexigenic response to tail pinch: role of brain NPY₁ and corticotropin releasing factor receptors

Goebel-Stengel

Stengel

Wang

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Tail pinch stimulates food intake in rats. We investigated brain mechanisms of this response and the influence of repeated exposure. Sprague-Dawley rats received acute (5 min) or repeated (5 min/day for 14 days) tail pinch using a padded clip. Acute tail pinch increased 5-min food intake compared with control (0.92 ± 0.2 vs. 0.03 ± 0.01 g, P < 0.01). This response was inhibited by 76% by intracerebroventricular injection of BIBP-3226, a neuropeptide Y1 (NPY1) receptor antagonist, increased by 48% by astressin-B, a corticotropin-releasing factor (CRF) receptor antagonist, and not modified by S-406-028, a somatostatin subtype 2 antagonist. After the 5-min tail pinch without food, blood glucose rose by 21% (P < 0.01) while changes in plasma acyl ghrelin (+41%) and adrenocorticotropic hormone (+37%) were not significant. Two tail pinches (45 min apart) activate pontine and hindbrain catecholaminergic and hypothalamic paraventricular CRF neurons. After 14 days of repeated tail pinch, the 5-min orexigenic response was not significantly different from days 2 to 11 but reduced by 50% thereafter (P < 0.001). Simultaneously, the 5-min fecal pellet output increased during the last 5 days compared with the first 5 days (+58%, P < 0.05). At day 14, the body weight gain was reduced by 22%, with a 99% inhibition of fat gain and a 25% reduction in lean mass (P < 0.05). The orexigenic response to acute 5-min tail pinch is likely to involve the activation of brain NPY1 signaling, whereas that of CRF tends to dampen the acute response and may contribute to increased defecation and decreased body weight gain induced by repeated tail pinch.

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Inhibition of food intake induced by acute stress in rats is due to satiation effects

Cited by 67 publications

References 59 publications

Preemptive Stimulation of AgRP Neurons in Fed Mice Enables Conditioned Food Seeking under Threat

Preemptive Stimulation of AgRP Neurons in Fed Mice Enables Conditioned Food Seeking under Threat

Hindbrain glucagon-like peptide-1 neurons track intake volume and contribute to injection stress-induced hypophagia in meal-entrained rats

Orexigenic response to tail pinch: role of brain NPY₁ and corticotropin releasing factor receptors

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Inhibition of food intake induced by acute stress in rats is due to satiation effects

Cited by 67 publications

References 59 publications

Preemptive Stimulation of AgRP Neurons in Fed Mice Enables Conditioned Food Seeking under Threat

Preemptive Stimulation of AgRP Neurons in Fed Mice Enables Conditioned Food Seeking under Threat

Hindbrain glucagon-like peptide-1 neurons track intake volume and contribute to injection stress-induced hypophagia in meal-entrained rats

Orexigenic response to tail pinch: role of brain NPY1 and corticotropin releasing factor receptors

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Orexigenic response to tail pinch: role of brain NPY₁ and corticotropin releasing factor receptors