Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P46098 (5-HT3 receptor)
 2,290 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism by which acid in the duodenum inhibits proximal gastric motor function and delays emptying was investigated in urethan-anesthetized and awake rats. Gastric motility inhibited by duodenal acid (0.2 N HCl) in urethan-anesthetized rats was attenuated by 68 and 54%, respectively, by functional ablation of the vagal or spinal sensory innervation with capsaicin. 5-Hydroxytryptamine3 receptor blockade with zacopride (0.2 mg/kg ip) or cholecystokinin (CCK)-A-type receptor blockade with MK-329 (1 mg/kg ip) had no effect on the motility response to acid. In awake rats with chronically implanted gastric and duodenal cannulas, perfusion of the duodenum with acid (0.1 and 0.2 N HCl) inhibited gastric emptying of a nonnutrient liquid (38 and 59%, respectively). Blockade of CCK-A-type receptors reduced by 30% inhibition of gastric emptying induced by 0.1 N HCl. However, functional ablation of the vagal or spinal sensory innervation, 5-hydroxytryptamine3 receptor blockade, or immunoneutralization of secretin by systemic administration of a polyclonal antibody (no. 7842, 1 ml ip) had no effect on acid-induced (0.1 N HCl) inhibition of gastric emptying. Perfusion of the duodenum with 0.2 N HCl but not 0.1 N HCl inhibited proximal gastric motility in awake rats. These results suggest that 1) a duodenal acid load inhibits gastric emptying in part by a mechanism involving CCK and 2) decreased proximal gastric motility plays a minor role in inhibition of gastric emptying in response to acid.
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PMID:Duodenal acid-induced inhibition of gastric motility and emptying in rats. 821 75

The present study investigated the relationship between endogenous CCK and serotonin (5-HT) in fat-induced satiety. Male Wistar rats with duodenal cannulas were adapted to eating 6 h/day along with receiving an infusion of saline or one of two isocaloric solutions (10 ml, 1 kcal/ml, 0.45 ml/min) varying in fat and carbohydrate content (20 or 80% energy from fat). Rats were infused 10 min after food presentation. The satiation/satiety response was determined from measures of meal size (MS), intermeal interval (IMI), and total food intake (TFI). Infusion with either fat solution reduced MS compared with saline; however, the 80% fat infusate reduced TFI and lengthened the IMI compared with saline and the 20% fat infusate. CCK and 5-HT involvement in fat-induced satiety was investigated by preceding the 80% fat infusate with CCK and/or 5-HT3 receptor antagonists Devazepide (Dev) and Tropisetron (Trop). A CCK releaser, trypsin inhibitor (TI), was added to the 20% fat infusate to enhance satiety. Pretreatment with Dev or Trop alone attenuated the inhibitory effects of the 80% solution on IMI, whereas reversal of the inhibitory effects on MS and TFI were sensitive only to Dev at the doses provided. Both antagonists together completely blocked the satiating effects of the 80% fat infusate on all feeding variables measured. Addition of TI to the 20% fat infusate lengthened the IMI but did not affect MS or TFI. These results provide evidence for the participation of both endogenous CCK and 5-HT in the satiety response to fat in the intestine.
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PMID:Cholecystokinin and serotonin receptors in the regulation of fat-induced satiety in rats. 995 Sep 21

Serotonin3 (5-HT3) receptors in the periphery mediate anorectic responses to the amino acid deficiency, which occurs after eating amino acid-imbalanced diets (IMB). However, other neurochemical systems, notably cholecystokinin (CCK), are known to affect food intake. We pretreated rats systemically with tropisetron, a 5-HT3 receptor antagonist, alone and combined with antagonists of CCK(A) and CCK(B) receptors, and measured intake of an IMB. Devazepide, a CCK(A) receptor antagonist, appeared to interact with tropisetron in the anorectic responses to IMB, blunting the usual remediation of IMB anorexia by tropisetron. The CCK(B) receptor antagonist, L-365, 260, increased intake of both IMB and an amino acid-balanced basal diet (BAS) and did not interact with tropisetron. Our data suggest that activation of CCK(A) receptors is interactive with 5-HT3 receptor activity in mediating IMB anorexia in the aminoprivic feeding model.
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PMID:CCK(A) and 5-HT3 receptors interact in anorectic responses to amino acid deficiency. 1008 Feb 41