Divergent circuitry underlying food reward and intake effects of ghrelin: Dopaminergic VTA-accumbens projection mediates ghrelin's effect on food reward but not food intake

Karolina Skibicka, Rozita H. Shirazi, Cristina Rabasa-Papio, Mayte Alvarez-Crespo, Corinna Neuber, Heike Vogel, Suzanne L. Dickson

Research output: Contribution to journalArticle

72 Citations (Scopus)

Abstract

Obesity has reached global epidemic proportions and creating an urgent need to understand mechanisms underlying excessive and uncontrolled food intake. Ghrelin, the only known circulating orexigenic hormone, potently increases food reward behavior. The neurochemical circuitry that links ghrelin to the mesolimbic reward system and to the increased food reward behavior remains unclear. Here we examine whether VTA-NAc dopaminergic signaling is required for the effects of ghrelin on food reward and intake. In addition, we examine the possibility of endogenous ghrelin acting on the VTA-NAc dopamine neurons. A D1-like or a D2 receptor antagonist was injected into the NAc in combination with ghrelin microinjection into the VTA to investigate whether this blockade attenuates ghrelin-induced food reward behavior. VTA injections of ghrelin produced a significant increase in food motivation/reward behavior, as measured by sucrose-induced progressive ratio operant conditioning, and chow intake. Pretreatment with either a D1-like or D2 receptor antagonist into the NAc, completely blocked the reward effect of ghrelin, leaving chow intake intact. We also found that this circuit is potentially relevant for the effects of endogenously released ghrelin as both antagonists reduced fasting (a state of high circulating levels of ghrelin) elevated sucrose-motivated behavior but not chow hyperphagia. Taken together our data identify the VTA to NAc dopaminergic projections, along with D1-like and D2 receptors in the NAc, as essential elements of the ghrelin responsive circuits controlling food reward behavior. Interestingly results also suggest that food reward behavior and simple intake of chow are controlled by divergent circuitry, where NAc dopamine plays an important role in food reward but not in food intake.

Original languageEnglish (US)
Pages (from-to)274-283
Number of pages10
JournalNeuropharmacology
Volume73
DOIs
StatePublished - Jan 1 2013

Fingerprint

Ghrelin
Reward
Eating
Food
Sucrose
Operant Conditioning
Hyperphagia
Dopaminergic Neurons
Microinjections
Motivation
Fasting
Dopamine
Obesity
Hormones

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Cellular and Molecular Neuroscience

Cite this

Skibicka, Karolina ; Shirazi, Rozita H. ; Rabasa-Papio, Cristina ; Alvarez-Crespo, Mayte ; Neuber, Corinna ; Vogel, Heike ; Dickson, Suzanne L. / Divergent circuitry underlying food reward and intake effects of ghrelin : Dopaminergic VTA-accumbens projection mediates ghrelin's effect on food reward but not food intake. In: Neuropharmacology. 2013 ; Vol. 73. pp. 274-283.
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abstract = "Obesity has reached global epidemic proportions and creating an urgent need to understand mechanisms underlying excessive and uncontrolled food intake. Ghrelin, the only known circulating orexigenic hormone, potently increases food reward behavior. The neurochemical circuitry that links ghrelin to the mesolimbic reward system and to the increased food reward behavior remains unclear. Here we examine whether VTA-NAc dopaminergic signaling is required for the effects of ghrelin on food reward and intake. In addition, we examine the possibility of endogenous ghrelin acting on the VTA-NAc dopamine neurons. A D1-like or a D2 receptor antagonist was injected into the NAc in combination with ghrelin microinjection into the VTA to investigate whether this blockade attenuates ghrelin-induced food reward behavior. VTA injections of ghrelin produced a significant increase in food motivation/reward behavior, as measured by sucrose-induced progressive ratio operant conditioning, and chow intake. Pretreatment with either a D1-like or D2 receptor antagonist into the NAc, completely blocked the reward effect of ghrelin, leaving chow intake intact. We also found that this circuit is potentially relevant for the effects of endogenously released ghrelin as both antagonists reduced fasting (a state of high circulating levels of ghrelin) elevated sucrose-motivated behavior but not chow hyperphagia. Taken together our data identify the VTA to NAc dopaminergic projections, along with D1-like and D2 receptors in the NAc, as essential elements of the ghrelin responsive circuits controlling food reward behavior. Interestingly results also suggest that food reward behavior and simple intake of chow are controlled by divergent circuitry, where NAc dopamine plays an important role in food reward but not in food intake.",
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Divergent circuitry underlying food reward and intake effects of ghrelin : Dopaminergic VTA-accumbens projection mediates ghrelin's effect on food reward but not food intake. / Skibicka, Karolina; Shirazi, Rozita H.; Rabasa-Papio, Cristina; Alvarez-Crespo, Mayte; Neuber, Corinna; Vogel, Heike; Dickson, Suzanne L.

In: Neuropharmacology, Vol. 73, 01.01.2013, p. 274-283.

Research output: Contribution to journalArticle

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AU - Skibicka, Karolina

AU - Shirazi, Rozita H.

AU - Rabasa-Papio, Cristina

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AU - Vogel, Heike

AU - Dickson, Suzanne L.

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AB - Obesity has reached global epidemic proportions and creating an urgent need to understand mechanisms underlying excessive and uncontrolled food intake. Ghrelin, the only known circulating orexigenic hormone, potently increases food reward behavior. The neurochemical circuitry that links ghrelin to the mesolimbic reward system and to the increased food reward behavior remains unclear. Here we examine whether VTA-NAc dopaminergic signaling is required for the effects of ghrelin on food reward and intake. In addition, we examine the possibility of endogenous ghrelin acting on the VTA-NAc dopamine neurons. A D1-like or a D2 receptor antagonist was injected into the NAc in combination with ghrelin microinjection into the VTA to investigate whether this blockade attenuates ghrelin-induced food reward behavior. VTA injections of ghrelin produced a significant increase in food motivation/reward behavior, as measured by sucrose-induced progressive ratio operant conditioning, and chow intake. Pretreatment with either a D1-like or D2 receptor antagonist into the NAc, completely blocked the reward effect of ghrelin, leaving chow intake intact. We also found that this circuit is potentially relevant for the effects of endogenously released ghrelin as both antagonists reduced fasting (a state of high circulating levels of ghrelin) elevated sucrose-motivated behavior but not chow hyperphagia. Taken together our data identify the VTA to NAc dopaminergic projections, along with D1-like and D2 receptors in the NAc, as essential elements of the ghrelin responsive circuits controlling food reward behavior. Interestingly results also suggest that food reward behavior and simple intake of chow are controlled by divergent circuitry, where NAc dopamine plays an important role in food reward but not in food intake.

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