Ingestion of a novel flavor before exposure to pups injected with lithium chloride produces a taste aversion in mother rats (Rattus norvegicus).

1984 ◽  
Vol 98 (3) ◽  
pp. 285-301 ◽  
Author(s):  
Gail A. Gemberling
1990 ◽  
Vol 68 (2) ◽  
pp. 269-278 ◽  
Author(s):  
Robert A. Fox ◽  
Merylee Corcoran ◽  
Kenneth R. Brizzee

The relationship between vomiting and conditioned taste aversion was studied in intact cats and squirrel monkeys and in cats and squirrel monkeys in which the area postrema was ablated by thermal cautery. In cats conditioned 7 – 12 months after ablation of the area postrema, three successive treatments with xylazine failed to produce either vomiting or conditioned taste aversion to a novel fluid. Intact cats, however, vomited and formed a conditioned aversion. In squirrel monkeys conditioned 6 months after ablation of the area postrema, three treatments with lithium chloride failed to produce conditioned taste aversion. Intact monkeys did condition with these treatments. Neither intact nor ablated monkeys vomited or evidenced other signs of illness when injected with lithium chloride. When the same ablated cats and monkeys were exposed to a form of motion that produced vomiting prior to surgery, conditioned taste aversion was produced and some animals vomited. These findings confirm other studies indicating motion can produce vomiting in animals with the area postrema destroyed and demonstrate that motion-induced conditioned taste aversion can be produced after ablation of the area postrema. The utility of conditioned taste aversion as a measure of subemetic motion sickness is discussed by examining agreement and disagreement between identifications of motion sickness by conditioned taste aversion and vomiting. It is suggested that a convincing demonstration of the utility of conditioned taste aversion as a measure of nausea requires the identification of physiological correlates of nausea, and caution should be exercised when attempting to interpret conditioned taste aversion as a measure of nausea.Key words: area postrema, conditioned taste aversion, motion sickness, nausea, emesis.


2015 ◽  
Vol 93 (2) ◽  
pp. 562-569 ◽  
Author(s):  
C. L. Manuelian ◽  
E. Albanell ◽  
M. Rovai ◽  
G. Caja ◽  
R. Guitart

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Tohru Hira ◽  
Shono Ogasawara ◽  
Hiroshi Hara

AbstractIntroductionDietary calcium has been proposed to reduce appetite (or to enhance satiety) in human studies. However, underlying mechanisms are still unclear. In animal and cell studies, it has been demonstrated that activation of the calcium-sensing receptor induced secretion of anorexic gut hormones such as cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) from enteroendocrine cells. In the present study, we tested the hypothesis that calcium suppresses appetite thorough enhanced gut hormone secretion, by using rats.Materials and MethodsMale Sprague Dawley rats were maintained by feeding a standard diet (AIN-93G, n = 6–8 per group). As calcium sources, calcium chloride, calcium carbonate, and calcium lactate were tested. These calcium salts were orally preloaded in fasted rats by using a feeding tube, and subsequent food intake was monitored until 24 hours. To assess conditioned taste aversion, saccharin preference test was conducted after conditioning with calcium or lithium chloride. To investigate involvements of gut hormones such as CCK, GLP-1, and peptide-YY (PYY), specific receptor antagonists for respective gut hormones were intraperitoneally injected just after oral preload of calcium, and then food intake was monitored. Portal blood samples were collected 15 or 30 min after oral preload of calcium for measurement of gut hormones by ELISA.Results and discussionAt the same dose of calcium (150 mg/kg), preload of calcium chloride reduced food intake for 4 hours compared to preload of the control solution (P < 0.05), while other compounds had minor effects on food intake. Saccharin preference ratio was only reduced by conditioning with lithium chloride (P < 0.01), but not by that with calcium compounds, indicating no conditional taste aversion was occurred by calcium. Suppressive effect of calcium chloride on food intake was partially reversed by pretreatment with a PYY receptor antagonist (BIIE0246) but not by that with a CCK- or a GLP-1 receptor antagonist. Portal PYY concentrations were higher in calcium chloride-treated rats than in the control rats (P < 0.05), 15 min after the preload and re-feeding. Changes in serum calcium concentrations were not observed by preload of calcium.These results suggest that oral preload of calcium chloride reduces subsequent food intake via enhanced PYY secretion in rats.


2012 ◽  
Vol 302 (11) ◽  
pp. R1351-R1363 ◽  
Author(s):  
Lindsey A. Schier ◽  
Terry L. Davidson ◽  
Terry L. Powley

In a previous report (Schier et al., Am J Physiol Regul Integr Comp Physiol 301: R1557–R1568, 2011), we demonstrated with a new behavioral procedure that rats exhibit stimulus-bound suppression of intake in response to an intraduodenal (ID) bitter tastant predicting subsequent malaise. With the use of the same modified taste aversion procedure, the present experiments evaluated whether the sweet taste properties of ID stimuli are likewise detected and encoded. Thirsty rats licked at sipper spouts for hypotonic NaCl for 30 min and received brief (first 6 min) yoked ID infusions of either the same NaCl or an isomolar lithium chloride (LiCl) solution in each session. An intestinal taste cue was mixed directly into the LiCl infusate for aversion training. Results showed that rats failed to detect intestinal sweet taste alone (20 mM Sucralose) but clearly suppressed licking in response to a nutritive sweet taste stimulus (234 mM sucrose) in the intestine that had been repeatedly paired with LiCl. Rats trained with ID sucrose in LiCl subsequently generalized responding to ID Sucralose alone at test. Replicating this, rats trained with ID Sucralose in compound with 80 mM Polycose rapidly suppressed licking to the 20 mM Sucralose alone in a later test. Furthermore, ID sweet taste signaling did not support the rapid negative feedback of sucrose or Polycose on intake when their digestion and transport were blocked. Together, these results suggest that other signaling pathways and/or transporters engaged by caloric carbohydrate stimuli potentiate detection of sweet taste signals in the intestine.


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