Excitatory amino acid receptor subtype agonists induce feeding in the nucleus accumbens shell in rats: opioid antagonist actions and interactions with μ-opioid agonists

Echo, Joyce A; Lamonte, Nicole; Christian, Garrison; Znamensky, Vladimir; Ackerman, Tsippa F.; Bodnar, Richard J.

doi:10.1016/s0006-8993(01)03094-3

Cited by 30 publications

(14 citation statements)

References 71 publications

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“…By extension then, our finding that the Gng3 Ϫ/Ϫ mice show reduced weight gain, decreased adiposity, reduced food intake, and attenuated fat preference is consistent with these animals harboring a defect in a reward pathway that responds to the pleasurable properties of palatable food. Craving for palatable food is considered as a form of addictive behavior (10,11,19,24,30), with the Oprm1 being strongly implicated in this process (8,47,48,50,52). Because Oprm1 represents the major molecular target of morphine in vivo (23,25,32,37,39), the attenuated responsiveness of Gng3 Ϫ/Ϫ mice to morphine is indicative of defective Oprm1 signaling.…”

Section: Discussionmentioning

confidence: 99%

“…Opioids promote the overconsumption of fat (47,50,51), and Oprm1 has been strongly implicated in this process (8,47,48,50,52). To determine whether the reduced fat preference of knockout mice was associated with a defect in -opioid signaling, we assessed the behavioral responsiveness of Gng3 Ϫ/Ϫ mice and their wild-type littermates to morphine, an opioid agonist that acts on the Oprm1 subtype (23,25,32,37,39).…”

Section: Gng3mentioning

confidence: 99%

“…Physiological studies have shown that consumption of fatty food increases the levels of endogenous opioids and -opioid receptor binding in discrete regions of the brain (6,36,44). Moreover, pharmacological studies have demonstrated that stereotactic injection of a -opioid agonist into the nucleus accumbens preferentially stimulates the intake of high-fat food (48,50,52), whereas an antagonist selectively blocks this response (8,48). Finally, gene-targeting studies have reported that mice lacking Oprm1 show increased weight gain on standard chow (12), reduced weight gain on a high-fat diet (38), diminished food anticipatory activity (15), decreased motivation to seek food (28), and attenuated psychomotor sensitization in response to morphine (49).…”

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confidence: 99%

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Mice lacking the G protein γ₃-subunit show resistance to opioids and diet induced obesity

Schwindinger

Borrell

Waldman

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Contributing to the obesity epidemic, there is increasing evidence that overconsumption of high-fat foods may be analogous to drug addiction in that the palatability of these foods is associated with activation of specific reward pathways in the brain. With this perspective, we report that mice lacking the G protein gamma(3)-subunit (Gng3(-/-) mice) show resistance to high-fat diet-induced weight gain over the course of a 12-wk study. Compared with Gng3(+/+) controls, female Gng3(-/-) mice exhibit a 40% reduction in weight gain and a 53% decrease in fat pad mass, whereas male Gng3(-/-) mice display an 18% reduction in weight gain and no significant decrease in fat pad mass. The basis for the lowered weight gain is related to reduced food consumption for female and male Gng3(-/-) mice of 13% and 14%, respectively. Female Gng3(-/-) mice also show a lesser preference for high-fat chow than their female Gng3(+/+) littermates, suggesting an attenuated effect on a reward pathway associated with overconsumption of fat. One possible candidate is the micro-opioid receptor (Oprm1) signaling cascade. Supporting a defect in this signaling pathway, Gng3(-/-) mice show marked reductions in both acute and chronic morphine responsiveness, as well as increases in endogenous opioid mRNA levels in reward-related regions of the brain. Taken together, these data suggest that the decreased weight gain of Gng3(-/-) mice may be related to a reduced rewarding effect of the high-fat diet resulting from a defect in Oprm1 signaling and loss of the G protein gamma(3)-subunit.

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Section: Discussionmentioning

confidence: 99%

Section: Gng3mentioning

confidence: 99%

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confidence: 99%

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Mice lacking the G protein γ₃-subunit show resistance to opioids and diet induced obesity

Schwindinger

Borrell

Waldman

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Another possibility for the mechanism of the apparent opioid interdependence is communication via other neurotransmitters. Opioids appear to interact with GABA in eliciting food intake from both the VTA and the sNAcc (3,32), and there are descending GABAergic pathways from the NAcc to the VTA directly (6,7,28) and indirectly via the hypothalamus (8). In fact, it has been shown that GABAergic cells in the NAcc, which project to the VTA and are inhibited by opioids in the NAcc, may decrease GABA release in the VTA, thereby creating a mechanism to explain NAcc opiate-triggered DA release from VTA cells (28,30).…”

Section: Discussionmentioning

confidence: 99%

Effects of the opioid antagonist naltrexone on feeding induced by DAMGO in the ventral tegmental area and in the nucleus accumbens shell region in the rat

MacDonald¹,

Billington²,

Levine³

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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. Effects of the opioid antagonist naltrexone on feeding induced by DAMGO in the ventral tegmental area and in the nucleus accumbens shell region in the rat. Am J Physiol Regul Integr Comp Physiol 285: R999-R1004, 2003. First published August 7, 2003 10.1152/ajpregu.00271. 2003.-The nucleus accumbens shell region (sNAcc) and the ventral tegmental area (VTA) are two major nodes in the mesolimbic dopamine pathway, which mediates reward for various survival behaviors, including feeding. Opioids increase and maintain food intake when injected peripherally and centrally. Opioids in the VTA cause increased release of dopamine in the sNAcc, and when injected into either site, cause an increase in food intake. Animals in this study were double cannulated in the VTA and in the sNAcc and injected with various combinations of naltrexone (NTX) (2.5, 5, and 25 g/side) and Tyr-D-Ala-Gly-(Me)Phe-Gly-ol (DAMGO) (0.1, 0.3, 1, 3, and 5 nmol/side) in both sites. DAMGO was found to dose dependently increase intake to an equal extent when injected into either site. DAMGO-induced increases in food intake when injected into the VTA were blocked to control levels with the highest dose of NTX injected bilaterally into the sNAcc; however, increases in intake when injected into the sNAcc were blocked only partially by the highest dose of NTX injected bilaterally into the VTA. These results indicate opioid-opioid communication between the two sites; however, the communication may be quite indirect, requiring other sites and transmitters to elicit a change in behavior. food intake; mesolimbic; microinjection; reward FOOD INTAKE results from the behavioral output of a diverse network of sites that integrates metabolic, emotional, and hedonic demands for increased or decreased consumption. Several peptides and neurotransmitters are responsible for different aspects of this behavior and appear to exert their effects differently in various brain sites (15). Opioids are thought to prolong intake, particularly of highly palatable foods, but not to initiate intake (9, 10), and this is not based on postabsorptive signals (11, 12). Opioid antagonists have been shown to inhibit intake of highly preferred foods much more robustly than less preferred foods, strengthening the argument that opioids are involved in the response to the quality of the food, rather than to hunger (16,29). Because opioids are also well-known hedonic agents, their actions in brain reward systems have been examined with regard to food intake.The ventral tegmental area (VTA) and the nucleus accumbens shell region (sNAcc) are part of the mesolimbic dopamine (DA) pathway that mediates responses to rewarding stimuli such as drugs of abuse, electrical stimulation, sex, and food intake (8). When opioids bind to their receptors in the VTA, they inhibit GABAergic inhibitory interneurons that synapse on DA cells projecting to the sNAcc. In this way, opioids injected or released into this site increase DA release in the sNAcc. This is thought to be part of the process that maintains f...

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“…Drug doses were chosen based on a literature review of prior work employing intracerebral injections of these drugs in behavioral testing situations. Doses that proved to have a behavioral effect formed the basis for the doses used in this experiment (Ranaldi and Benninger, 1994;Maldonado-Irizarry et al, 1995;Echo et al, 2001;Ikeda et al, 2003;Moribe et al, 2005;Uchida et al, 2005;Eiler et al, 2006;Ansah et al, 2007). The drugs were all dissolved in saline and the pH of each solution was titrated to 7.2-7.4.…”

Section: Methodsmentioning

confidence: 99%

Brain stimulation reward is altered by affecting dopamine–glutamate interactions in the central extended amygdala

Waraczynski¹,

Zwifelhofer²,

Kuehn³

2012

Neuroscience

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Excitatory amino acid receptor subtype agonists induce feeding in the nucleus accumbens shell in rats: opioid antagonist actions and interactions with μ-opioid agonists

Cited by 30 publications

References 71 publications

Mice lacking the G protein γ₃-subunit show resistance to opioids and diet induced obesity

Mice lacking the G protein γ₃-subunit show resistance to opioids and diet induced obesity

Effects of the opioid antagonist naltrexone on feeding induced by DAMGO in the ventral tegmental area and in the nucleus accumbens shell region in the rat

Brain stimulation reward is altered by affecting dopamine–glutamate interactions in the central extended amygdala

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Excitatory amino acid receptor subtype agonists induce feeding in the nucleus accumbens shell in rats: opioid antagonist actions and interactions with μ-opioid agonists

Cited by 30 publications

References 71 publications

Mice lacking the G protein γ3-subunit show resistance to opioids and diet induced obesity

Mice lacking the G protein γ3-subunit show resistance to opioids and diet induced obesity

Effects of the opioid antagonist naltrexone on feeding induced by DAMGO in the ventral tegmental area and in the nucleus accumbens shell region in the rat

Brain stimulation reward is altered by affecting dopamine–glutamate interactions in the central extended amygdala

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Resources

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Mice lacking the G protein γ₃-subunit show resistance to opioids and diet induced obesity

Mice lacking the G protein γ₃-subunit show resistance to opioids and diet induced obesity