ArticlePsychoneuroendocrinology2014
Peripheral α2-β1 adrenergic interactions mediate the ghrelin response to brain urocortin 1 in rats.
Article in Psychoneuroendocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Evidence for independent actions of the CRF and ghrelin systems in binge-like alcohol drinking in mice.Progress in neuro-psychopharmacology & biological psychiatry · 2025Article
- Treatment of Gastrointestinal Disorders-Plants and Potential Mechanisms of Action of Their Constituents.Molecules (Basel, Switzerland) · 2022Review
- Ghrelin Enhancer, the Latest Evidence of Rikkunshito.Frontiers in nutrition · 2021Review
- Vulnerability to psychological stress-induced anorexia in female mice depends on blockade of ghrelin signal in nucleus tractus solitarius.British journal of pharmacology · 2020Article
- Usefulness of a Kampo Medicine on Stress-Induced Delayed Gastric Emptying in Mice.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Ghrelin enhancer, rikkunshito, improves postprandial gastric motor dysfunction in an experimental stress model.Neurogastroenterology and motility · 2015Article
- Rikkunshito, a ghrelin potentiator, ameliorates anorexia-cachexia syndrome.Frontiers in pharmacology · 2014Review
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Authors and funding
9 authors at 5 institutions in 2 countries.
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Abstract
The autonomic nervous system (ANS) conveys neuronal input from the brain to the stomach. We investigated mechanisms through which urocortin 1 (UCN1) injected intracerebroventricularly (ICV, 300 pmol/rat) inhibits circulating ghrelin in rats. This was achieved by assessing (1) the induction of c-fos gene expression as a marker of neuronal activation in specific hypothalamic and caudal brainstem regulating ANS; (2) the influence of vagotomy and pharmacological blockade of central and peripheral α- and β-adrenergic receptor (AR) on ICV UCN1-induced reduction of plasma ghrelin levels (determined by ELISA); and (3) the relevance of this pathway in the feeding response to a fast in rats. UCN1 increased c-fos mRNA expression in key brain sites influencing sympathetic activity namely the hypothalamic paraventricular and ventromedial nuclei, locus coeruleus, nucleus of the solitary tract, and rostral ventrolateral medulla, by 16-, 29-, 6-, 37-, and 13-fold, respectively. In contrast, the dorsal motor nucleus of the vagus had little c-fos mRNA expression and ICV UCN1 induced a similar reduction in acylated ghrelin in the sham-operated (31%) and vagotomized (41%) rats. An intraperitoneal (IP) injection of either a non-selective α- or selective α2-AR antagonist reduced, while a selective α2-AR agonist enhanced ICV UCN1-induced suppression of plasma acylated ghrelin levels. In addition, IP injection of a non-selective β- or selective β1-AR agonist blocked, and selective β1-AR antagonist augmented, the ghrelin response to ICV UCN1. The IP injections of a selective α1- or non-selective β or β2-AR antagonists, or any of the pretreatments given ICV had no effect. ICV UCN1 reduced the 2-h food intake in response to a fast by 80%, and this effect was partially prevented by a selective α2-AR antagonist. These data suggest that ICV UCN1 reduces plasma ghrelin mainly through the brain sympathetic component of the ANS and peripheral AR specifically α2-AR activation and inactivation of β1-AR. The α2-AR pathway contributes to the associated reduction in food intake.
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