scholarly journals Ghrelin increases the motivation to eat, but does not alter food palatability

2012 ◽  
Vol 303 (3) ◽  
pp. R259-R269 ◽  
Author(s):  
Joost Overduin ◽  
Dianne P. Figlewicz ◽  
Jennifer Bennett-Jay ◽  
Sepideh Kittleson ◽  
David E. Cummings
Keyword(s):  
Energy Intake ◽  
Food Reward ◽  
Sch 23390 ◽  
Progressive Ratio ◽  
Lick Rate ◽  
Positive Control ◽  
D1 Receptor ◽  
Gastrointestinal Hormone ◽  
Hedonic Valuation ◽  
Lever Pressing

Homeostatic eating cannot explain overconsumption of food and pathological weight gain. A more likely factor promoting excessive eating is food reward and its representation in the central nervous system (CNS). The anorectic hormones leptin and insulin reduce food reward and inhibit related CNS reward pathways. Conversely, the orexigenic gastrointestinal hormone ghrelin activates both homeostatic and reward-related neurocircuits. The current studies were conducted to identify in rats the effects of intracerebroventricular ghrelin infusions on two distinct aspects of food reward: hedonic valuation (i.e., “liking”) and the motivation to self-administer (i.e., “wanting”) food. To assess hedonic valuation of liquid food, lick motor patterns were recorded using lickometry. Although ghrelin administration increased energy intake, it did not alter the avidity of licking (initial lick rates or lick-cluster size). Several positive-control conditions ruled out lick-rate ceiling effects. Similarly, when the liquid diet was hedonically devalued with quinine supplementation, ghrelin failed to reverse the quinine-associated reduction of energy intake and avidity of licking. The effects of ghrelin on rats' motivation to eat were assessed using lever pressing to self-administer food in a progressive-ratio paradigm. Ghrelin markedly increased motivation to eat, to levels comparable to or greater than those seen following 24 h of food deprivation. Pretreatment with the dopamine D1 receptor antagonist SCH-23390 eliminated ghrelin-induced increases in lever pressing, without compromising generalized licking motor control, indicating a role for D1 signaling in ghrelin's motivational feeding effects. These results indicate that ghrelin increases the motivation to eat via D1 receptor-dependent mechanisms, without affecting perceived food palatability.

The D1 receptor antagonist, SCH 23390, induces signs of parkinsonism in African green monkeys

Life Sciences ◽  
1991 ◽  
Vol 49 (25) ◽  
pp. PL229-PL234 ◽  
Author(s):  
Matthew S. Lawrence ◽  
D.Eugene Redmond ◽  
J.D. Elsworth ◽  
J.R. Taylor ◽  
R.H. Roth
Keyword(s):  
Receptor Antagonist ◽  
Sch 23390 ◽  
D1 Receptor ◽  
D1 Receptor Antagonist ◽  
Green Monkeys

scholarly journals Enhanced food motivation in obese mice is controlled by D1R expressing spiny projection neurons in the nucleus accumbens.

2022 ◽  
Author(s):  
Bridget A Matikainen-Ankney ◽  
Alex A Legaria ◽  
Yvan M Vachez ◽  
Caitlin A Murphy ◽  
Yiyan A Pan ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Food Reward ◽  
Ex Vivo ◽  
D1 Receptor ◽  
Physical Work ◽  
Projection Neurons ◽  
Food Motivation ◽  
Obese Mice ◽  
Food Seeking

Obesity is a chronic relapsing disorder that is caused by an excess of caloric intake relative to energy expenditure. In addition to homeostatic feeding mechanisms, there is growing recognition of the involvement of food reward and motivation in the development of obesity. However, it remains unclear how brain circuits that control food reward and motivation are altered in obese animals. Here, we tested the hypothesis that signaling through pro-motivational circuits in the core of the nucleus accumbens (NAc) is enhanced in the obese state, leading to invigoration of food seeking. Using a novel behavioral assay that quantifies physical work during food seeking, we confirmed that obese mice work harder than lean mice to obtain food, consistent with an increase in the relative reinforcing value of food in the obese state. To explain this behavioral finding, we recorded neural activity in the NAc core with both in vivo electrophysiology and cell-type specific calcium fiber photometry. Here we observed greater activation of D1-receptor expressing NAc spiny projection neurons (NAc D1SPNs) during food seeking in obese mice relative to lean mice. With ex vivo slice physiology we identified both pre- and post-synaptic mechanisms that contribute to this enhancement in NAc D1SPN activity in obese mice. Finally, blocking synaptic transmission from D1SPNs decreased physical work during food seeking and attenuated high-fat diet-induced weight gain. These experiments demonstrate that obesity is associated with a selective increase in the activity of D1SPNs during food seeking, which enhances the vigor of food seeking. This work also establishes the necessity of D1SPNs in the development of diet-induced obesity, identifying a novel potential therapeutic target.

scholarly journals Measurement of Cortical Dopamine D1 Receptor Binding with [11C]SCH 23390: A Test–Retest Analysis

2001 ◽  
Vol 21 (10) ◽  
pp. 1146-1150 ◽  
Author(s):  
Jussi Hirvonen ◽  
Kjell Någren ◽  
Jaana Kajander ◽  
Jarmo Hietala
Keyword(s):  
Sch 23390 ◽  
Intraclass Correlation ◽  
Three Dimensional ◽  
Correlation Coefficients ◽  
D1 Receptor ◽  
Binding Potential ◽  
Intraclass Correlation Coefficients ◽  
Cortical Areas ◽  
Scan Time ◽  
Positron Emission

[11C]SCH 23390 is a standard ligand for positron emission tomography (PET) studies on striatal dopamine D1 receptors. Its usefulness for cortical D1 receptor quantification in human PET studies has been questioned but has not been addressed previously. The authors tested the reproducibility of [11C]SCH 23390 binding potential (BP) in cortical areas in five healthy volunteers using three-dimensional PET. Measurement of D1 receptor BP was reproducible in basal ganglia, as well as in all cortical areas studied (intraclass correlation coefficients between 0.81 and 0.92). The absolute variability in cortical areas was 9.21% ± 0.07%. The reproducibility of cortical D1 receptor BP measurement with [11C]SCH 23390 is equal to that observed with a more recent D1 -ligand, [11C]NNC 112. [11C]NNC 112 produces slightly higher specific-to-nonspecific binding ratios but has markedly slower kinetics resulting in a need for a longer scan time. These aspects should be considered when designing studies on the cortical D1 -like receptors.

scholarly journals Tryptophan-Tyrosine Dipeptide, the Core Sequence of β-Lactolin, Improves Memory by Modulating the Dopamine System

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 348 ◽  
Author(s):  
Yasuhisa Ano ◽  
Tatsuhiro Ayabe ◽  
Rena Ohya ◽  
Keiji Kondo ◽  
Shiho Kitaoka ◽  
...  
Keyword(s):  
Sch 23390 ◽  
D1 Receptor ◽  
Memory Impairments ◽  
The Core ◽  
Core Sequence ◽  
Maze Test ◽  
Age Related ◽  
Y Maze ◽  
Age Related Cognitive Decline

Tryptophan-tyrosine (WY)-related peptides including the β-lactopeptide of the glycine-threonine-tryptophan-tyrosine peptide, β-lactolin, improve spatial memory. However, whether and how the WY dipeptide as the core sequence in WY-related peptides improves memory functions has not been investigated. This study assessed the pharmacological effects of the WY dipeptide on memory impairment to elucidate the mechanisms. Here, we showed that oral administration of dipeptides of WY, tryptophan-methionine (WM), tryptophan-valine, tryptophan-leucine, and tryptophan-phenylalanine improved spontaneous alternation of the Y-maze test in scopolamine-induced amnesic mice. In contrast, tyrosine-tryptophan, methionine-tryptophan, tryptophan, tyrosine, and methionine had no effect. These results indicated that the conformation of dipeptides with N-terminal tryptophan is required for their memory improving effects. WY dipeptide inhibited the monoamine oxidase B activity in vitro and increased dopamine levels in the hippocampus and frontal cortex, whereas tryptophan did not cause these effects. In addition, the treatment with SCH-23390, a dopamine D1-like receptor antagonist, and the knockdown of the hippocampal dopamine D1 receptor partially attenuated the memory improvement induced by the WY dipeptide. Importantly, WY dipeptide improved the spontaneous alternations of the Y-maze test in aged mice. These results suggest that the WY dipeptide restores memory impairments by augmenting dopaminergic activity. The development of supplements rich in these peptides might help to prevent age-related cognitive decline.

scholarly journals Effect of exercise-meal timing on energy intake, appetite and food reward in adolescents with obesity: The TIMEX study

Appetite ◽  
2020 ◽  
Vol 146 ◽  
pp. 104506 ◽  
Author(s):  
A. Fillon ◽  
M.E. Mathieu ◽  
J. Masurier ◽  
J. Roche ◽  
M. Miguet ◽  
...  
Keyword(s):  
Energy Intake ◽  
Food Reward ◽  
Meal Timing

Dopamine D1 receptor antagonist inhibits swallowing reflex in guinea pigs

1998 ◽  
Vol 274 (1) ◽  
pp. R76-R80 ◽  
Author(s):  
Yu Xia Jia ◽  
Kiyohisa Sekizawa ◽  
Takashi Ohrui ◽  
Katsutoshi Nakayama ◽  
Hidetada Sasaki
Keyword(s):  
Receptor Antagonist ◽  
Guinea Pigs ◽  
Sch 23390 ◽  
Specific Inhibitor ◽  
Visual Observation ◽  
D1 Receptor ◽  
Electromyographic Activity ◽  
Distilled Water ◽  
Peripheral Organs ◽  
Swallowing Reflex

To determine whether dopamine D1receptor antagonist impairs the swallowing reflex and reduces substance P (SP) in the peripheral organs, the swallowing reflex in terms of the number of swallows elicited by injections of three different volumes (0.2, 0.4, and 0.6 ml) of distilled water into the pharynx through a catheter was examined in anesthetized guinea pigs pretreated with Sch-23390. Animals were pretreated with either subcutaneous Sch-23390 (200 μg/kg) or a vehicle of Sch-23390 every 12 h for 7 days. The number of swallows was counted by submental electromyographic activity and visual observation of characteristic laryngeal movement. Injections of distilled water caused a volume-dependent increase in the number of swallows in animals without Sch-23390 treatment. Sch-23390 significantly decreased and exogenously administered SP increased the number of swallows elicited by all volumes of distilled water. FK-888 (10−5 M, 1 ml), a specific inhibitor of the NK1 receptor, reduced the number of swallows to a greater degree than Sch-23390. Sch-23390 significantly reduced SP content in the laryngeal and pharyngeal mucosa compared with control. These results suggest that inhibition of the dopamine D1 receptor may impair the swallowing reflex and reduce SP content in the peripheral organs.

Load-dependent effects of duodenal glucose on glycemia, gastrointestinal hormones, antropyloroduodenal motility, and energy intake in healthy men

2007 ◽  
Vol 293 (3) ◽  
pp. E743-E753 ◽  
Author(s):  
Amelia N. Pilichiewicz ◽  
Reawika Chaikomin ◽  
Ixchel M. Brennan ◽  
Judith M. Wishart ◽  
Christopher K. Rayner ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Energy Intake ◽  
Healthy Subjects ◽  
Gastrointestinal Hormones ◽  
Saline Control ◽  
Gastrointestinal Hormone ◽  
Double Blind ◽  
Glucagon Like Peptide 1 ◽  
Glucose Plasma

Gastric emptying is a major determinant of glycemia, gastrointestinal hormone release, and appetite. We determined the effects of different intraduodenal glucose loads on glycemia, insulinemia, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and cholecystokinin (CCK), antropyloroduodenal motility, and energy intake in healthy subjects. Blood glucose, plasma hormone, and antropyloroduodenal motor responses to 120-min intraduodenal infusions of glucose at 1) 1 (“G1”), 2) 2 (“G2”), and 3) 4 (“G4”) kcal/min or of 4) saline (“control”) were measured in 10 healthy males in double-blind, randomized fashion. Immediately after each infusion, energy intake at a buffet meal was quantified. Blood glucose rose in response to all glucose infusions ( P < 0.05 vs. control), with the effect of G4 and G2 being greater than that of G1 ( P < 0.05) but with no difference between G2 and G4. The rises in insulin, GLP-1, GIP, and CCK were related to the glucose load ( r > 0.82, P < 0.05). All glucose infusions suppressed antral ( P < 0.05), but only G4 decreased duodenal, pressure waves ( P < 0.01), resulted in a sustained stimulation of basal pyloric pressure ( P < 0.01), and decreased energy intake ( P < 0.05). In conclusion, variations in duodenal glucose loads have differential effects on blood glucose, plasma insulin, GLP-1, GIP and CCK, antropyloroduodenal motility, and energy intake in healthy subjects. These observations have implications for strategies to minimize postprandial glycemic excursions in type 2 diabetes.

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