Sugar appetite is influenced by unlearned attractions to sweet taste and learned responses to sugars' taste and post-ingestive actions. In rats, sugar-conditioned flavor preferences (CFP) are attenuated by dopamine D1 (SCH23390: SCH), but not by opioid (naltrexone: NTX), receptor antagonism. Sucrose-CFP occurs in BALB/c and SWR inbred mice that differ in their suppressive effects of SCH and NTX on sucrose intake. The present study examined whether SCH and NTX altered expression of previously learned sucrose-CFP and acquisition (learning) of sucrose-CFP in these strains. In Experiment 1, food-restricted mice were trained (10 one-bottle sessions) to drink a more-preferred flavored (e.g., cherry) 16% sucrose solution (CS+/Sucrose) on odd-numbered days, and a less-preferred flavored (e.g., grape) 0.05% saccharin solution (CS-/Saccharin) on even-numbered days. Two-bottle tests with the flavors mixed in 0.2% saccharin occurred 30 min following vehicle (Veh), SCH (50-800 nmol/kg) or NTX (1-5mg/kg) assessing preference expression. CS+ preference expression in BALB/c and SWR mice following Veh were significantly reduced by SCH and NTX. In Experiment 2, separate groups of BALB/c and SWR mice received Veh, SCH (50 nmol/kg) or NTX (1mg/kg) injections 30 min prior to daily one-bottle training sessions with the CS+/Sucrose and CS-/Saccharin solutions assessing preference acquisition. Subsequent two-bottle tests with the CS+ vs. CS- solutions were conducted without injections. CS+/Sucrose training intakes were reduced by SCH in both strains and by NTX in BALB/c mice. In the initial two-bottle test, sucrose-CFP acquisition was significantly reduced in BALB NTX (54%), but not in BALB SCH (77%) groups relative to the BALB Veh group (85%). In contrast, sucrose-CFP acquisition was significantly reduced in SWR SCH (61%), but not in SWR NTX (83%) groups relative to the SWR Veh group (86%). DA D1 and opioid receptor signaling modulate acquisition and/or expression of sucrose-CFP in mice with significant strain differences observed.
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http://dx.doi.org/10.1016/j.pbb.2012.07.018 | DOI Listing |
Transgenic Res
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Department of Pathology, FARAH, Faculty of Veterinary Medicine, University of Liege, Liège, Belgium.
Mice are the most widely used mammalian animal model worldwide. Their use presents many advantages, including our ability to manipulate their genome. Unfortunately, transgenic mice often need to be introgressed to transfer the transgene of interest in a specific mouse line.
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Department of Psychology, Queens College, CUNY, 65-30 Kissena Blvd., Flushing, NY 11367, United States; Psychology Doctoral Program and CUNY Neuroscience Collaborative, CUNY, United States. Electronic address:
Inbred mouse strains differ in their postoral appetite stimulating response (appetition) to fructose as demonstrated in intragastric (IG) sugar conditioning and oral sugar vs. nonnutritive conditioning experiments. For example, FVB and SWR strains show experience-induced preferences for 8% fructose over a 0.
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November 2021
Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
Background: Obesity is a risk factor for the development of asthma. However, pharmacologic therapeutic strategies that specifically target obese asthmatics have not been identified. We hypothesize that glucagon-like peptide-1 receptor agonist (GLP-1RA) treatment inhibits aeroallergen-induced early innate airway inflammation in a mouse model of asthma in the setting of obesity.
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Department of Biology, University of Kentucky, Lexington, Kentucky.
Physiol Behav
October 2020
Department of Psychology, Queens College, City University of New York (CUNY); CUNY Neuroscience Collaborative and Psychology Doctoral Program, CUNY Graduate Center, New York, NY, USA. Electronic address:
Dopamine, opioid and muscarinic receptor antagonists differentially reduce sucrose and saccharin intakes across inbred mouse strains. Whereas these systems stimulate sweet intake, serotonin signaling inhibits food intake. The present study examined whether fluoxetine (0.
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