The induction and suppression of c-fos expression in the rat brain by cholecystokinin and its antagonist L364,718

Chen, Dong‐Yi; Deutsch, J. A.; Gonzalez, Manuel F.; Gu, Yin

doi:10.1016/0304-3940(93)90355-o

Cited by 84 publications

(46 citation statements)

References 20 publications

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“…The HPA axis is directly sensitive to CCK activation (Kamilaris et al 1992;Matsumura et al 1983;Mezey et al 1986;Reisine and Jensen 1986). Central CCK systems are sensitive to levels of stress and circulating glucocorticoids (Mezey et al 1986;Siegel et al 1987) and peripheral CCK can regulate activity in central components of the HPA axis (Chen et al 1993).…”

Section: Discussionmentioning

confidence: 99%

Dose Response of Adrenocorticotropin and Cortisol to the CCK-B Agonist Pentagastrin

Abelson

Liberzon

1999

Neuropsychopharmacology

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Section: Discussionmentioning

confidence: 99%

Dose Response of Adrenocorticotropin and Cortisol to the CCK-B Agonist Pentagastrin

Abelson

Liberzon

1999

Neuropsychopharmacology

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“…Studies investigating the role of CCK-1 receptors in activation of the NTS using selective receptor agonist and antagonist have yielded conflicting data (12,28,71). Also, lesions of the NTS block or attenuate the satiety effect of CCK (24).…”

Section: Perspectivesmentioning

confidence: 99%

Independent ingestion and microstructure of feeding patterns in infant rats lacking CCK-1 receptors

Blumberg

Haba²,

Schroêder³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Otsuka Long-Evans Tokushima fatty (OLETF) rats are a strain of Long-Evans Tokushima Otsuka (LETO) rats that do not express CCK-1 receptors, developing in adulthood, hyperphagia, obesity, and non-insulin-dependent diabetes mellitus (NIDDM). We examined weight gain and meal patterns during a 30-min independent ingestion test on postnatal days 2-4 and again on days 9 -11 in OLETF and LETO rat pups. OLETF pups were significantly heavier compared with their LETO controls at both ages, and they consumed significantly more of the sweet milk diet. The difference in intake can be attributed to a significant increase in meal size and duration. Number of clusters and bursts of licking within a meal were greater in OLETF rat pups, with no difference between strains in burst and cluster size. Interlick interval (ILI) was not significantly different between OLETF and LETO pups. This measure decreased on days 9 -11 compared with days 2-4 in both strains. Latency to start feeding was significantly shorter on days 2-4 in OLETF vs. LETO pups, but this difference disappeared at the second test at the older age. Two-to four-day-old OLETF pups consumed a larger volume of milk during the first minute of feeding, and their initial lick rate and decay of lick rate were significantly larger compared with their LETO controls. Lack of CCK-1 receptors, or other OLETF-related abnormalities, therefore, resulted in a satiation deficit, leading to increased meal size, hyperphagia, and increased weight gain as early as 2-4 postnatal days. cholecystokinin; obesity; independent ingestion; meal-patterns; Otsuka Long-Evans Tokushima fatty rats; infant rats THE BRAIN-GUT PEPTIDE CHOLECYSTOKININ (CCK) has been demonstrated to reduce food intake in a dose-related manner in different species and experimental designs (3,29,35). Entry of food into the intestine triggers the release of endogenous CCK by the intestinal mucosa, thereby activating CCK-1 receptors located in the periphery to transmit through the vagus nerve a neural signal to the brain, which subsequently terminates feeding and initiates the sequence of behaviors associated with satiety (4, 60).CCK was found to reduce meal size and duration (29, 38) and to induce an earlier appearance of behavioral satiety. The satiety produced by endogenous or exogenous administration of the peptide is mediated via interaction with CCK-1 receptors rather than CCK-2 receptors (5, 44). CCK-1 receptors are abundant in peripheral organs and in a few discrete brain regions (33, 45).Exogenous and endogenous CCK, through receptors of CCK-1, have been shown to reduce feeding in newborn and infant rats independently ingesting their first meal away from the dam (53, 61, 68). Furthermore, CCK-1 receptors appear to mediate a portion of the reduction of intake produced by a preload of corn oil (but not by mineral oil, glucose, 2-deoxy-D-glucose, maltose, or peptone) in infant rats (66 -69). These findings suggest that the CCK system can function selectively at a preweanling age, mediating the emerging feeding-regulatory ...

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“…Intraluminal products of lipid digestion stimulate the release of CCK from intestinal enteroendocrine cells (10,13,18). Postprandially released CCK, in turn, acts on CCK 1 receptors (CCK 1 Rs) on vagal afferent nerve terminals in the intestinal mucosa (2), which, in turn, results in stimulation of neurons in the nucleus of the solitary tract (NTS) (4,6,19), a brain region involved in the regulation of proximal gastrointestinal function and food intake.…”

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confidence: 99%

Targeted disruption of the murine CCK₁ receptor gene reduces intestinal lipid-induced feedback inhibition of gastric function

Whited¹,

Thao²,

Lloyd³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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The induction and suppression of c-fos expression in the rat brain by cholecystokinin and its antagonist L364,718

Cited by 84 publications

References 20 publications

Dose Response of Adrenocorticotropin and Cortisol to the CCK-B Agonist Pentagastrin

Dose Response of Adrenocorticotropin and Cortisol to the CCK-B Agonist Pentagastrin

Independent ingestion and microstructure of feeding patterns in infant rats lacking CCK-1 receptors

Targeted disruption of the murine CCK₁ receptor gene reduces intestinal lipid-induced feedback inhibition of gastric function

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The induction and suppression of c-fos expression in the rat brain by cholecystokinin and its antagonist L364,718

Cited by 84 publications

References 20 publications

Dose Response of Adrenocorticotropin and Cortisol to the CCK-B Agonist Pentagastrin

Dose Response of Adrenocorticotropin and Cortisol to the CCK-B Agonist Pentagastrin

Independent ingestion and microstructure of feeding patterns in infant rats lacking CCK-1 receptors

Targeted disruption of the murine CCK1 receptor gene reduces intestinal lipid-induced feedback inhibition of gastric function

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Targeted disruption of the murine CCK₁ receptor gene reduces intestinal lipid-induced feedback inhibition of gastric function