Feeding elicited by dynorphin (1–13) microinjections into the ventral tegmental area in rats

Hamilton, Margaret E.; Bozarth, Michael A.

doi:10.1016/0024-3205(88)90271-8

Cited by 61 publications

(17 citation statements)

References 24 publications

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“…Early studies demonstrated that microinjections of morphine or an enkephalin analogue into the VTA or NAc promote food intake in rats (Mucha & Iversen, 1986;Jenck et al, 1987;Hamilton & Bozarth, 1988). These effects are blocked by locally injected mu-opioid receptor antagonists (Kelley et al, 1996;Will et al, 2006;Katsuura & Taha, 2014).…”

Section: Mu-opioid Receptor Involvement In Feeding Behaviourmentioning

confidence: 96%

“…"Liking" refers to the perceived palatability of a food or the hedonic pleasure an animal derives from eating, whereas "wanting" refers to the motivation to consume. Agonists of the mu-opioid receptor can increase food "wanting" as shown by increased food consumption (Jenck et al, 1987;Hamilton & Bozarth, 1988;MacDonald et al, 2004). Food "wanting" involves dopamine (Peciña et al, 2003).…”

Section: Mu-opioid Receptor Involvement In Feeding Behaviourmentioning

confidence: 99%

See 1 more Smart Citation

Changes in mu-opioid receptor expression and function in the mesolimbic system after long-term access to a palatable diet

Pitman

Borgland

2015

Pharmacology & Therapeutics

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Section: Mu-opioid Receptor Involvement In Feeding Behaviourmentioning

confidence: 96%

Section: Mu-opioid Receptor Involvement In Feeding Behaviourmentioning

confidence: 99%

Changes in mu-opioid receptor expression and function in the mesolimbic system after long-term access to a palatable diet

Pitman

Borgland

2015

Pharmacology & Therapeutics

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“…At this point in time, two brain sites have been identified by which the dynorphin-like peptides may increase food intake. The administration of dynorphin A into the medial hypothalamus and the ventral tegmental area has been shown to increase food intake in rats (Gosnell, 1988) (Hamilton and Bozarth, 1988). Dynorphin A (1-13) binds with a high affinity to kappa-opioid receptors but also with a low affinity to mu-opioid receptors and therefore the dose-response curves of dynorphin A (1-13) and the mu-opioid receptor agonist morphine were compared.…”

Section: Kappa-opioid Receptor Ligands and Behaviormentioning

confidence: 99%

kappa-Opioid receptor signaling and brain reward function

Bruijnzeel

2009

Brain Research Reviews

175

121

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The dynorphin-like peptides have profound effects on the state of the brain reward system and human and animal behavior. The dynorphin-like peptides affect locomotor activity, food intake, sexual behavior, anxiety-like behavior, and drug intake. Stimulation of kappa-opioid receptors, the endogenous receptor for the dynorphin-like peptides, inhibits dopamine release in the striatum (nucleus accumbens and caudate putamen) and induces a negative mood state in humans and animals. The administration of drugs of abuse increases the release of dopamine in the striatum and mediates the concomitant release of dynorphin-like peptides in this brain region. The reviewed studies suggest that chronic drug intake leads to an upregulation of the brain dynorphin system in the striatum and in particular in the dorsal part of the striatum/caudate putamen. This might inhibit drug-induced dopamine release and provide protection against the neurotoxic effects of high dopamine levels. After the discontinuation of chronic drug intake these neuroadaptations remain unopposed which has been suggested to contribute to the negative emotional state associated with drug withdrawal and increased drug intake. Kappa-opioid receptor agonists have also been shown to inhibit calcium channels. Calcium channel inhibitors have antidepressant-like effects and inhibit the release of norepinephrine. This might explain that in some studies kappa-opioid receptor agonists attenuate nicotine and opioid withdrawal symptomatology. A better understanding of the role of dynorphins in the regulation of brain reward function might contribute to the development of novel treatments for mood disorders and other disorders that stem from a dysregulation of the brain reward system.

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“…It is noteworthy that our studies specifically focused on the disruption of dynorphins. Dynorphins activate all three types of opioid receptors (µ, δ and κ), but bind with much higher preference for κ-opioid receptors (Hamilton and Bozarth, 1988), which have been implicated in the regulation of energy homeostasis (Arjune and Bodnar, 1990, Hamilton and Bozarth, 1988and Levine et al, 1990. It is possible that other endogenous opioid system peptides, the endorphins and enkephalins, could functionally compensate for the absence of dynorphin function.…”

Section: Discussionmentioning

confidence: 99%

“…Of these endogenous opioid systems, κ opioid receptors have been particularly implicated in these processes (Arjune and Bodnar, 1990, Hamilton and Bozarth, 1988and Levine et al, 1990. Specific blockade of κ-opioid receptors significantly reduces fasting-induced hyperphagia in rats (Lambert et al, 1993), as well as food intake and body weight in obese rodent models (Cole et al, 1995 andJarosz andMetzger, 2002).…”

Section: Introductionmentioning

confidence: 99%

Double deletion of orexigenic neuropeptide Y and dynorphin results in paradoxical obesity in mice

et al. 2014

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ObjectiveOrexigenic neuropeptide Y (NPY) and dynorphin (DYN) regulate energy homeostasis. Single NPY or dynorphin deletion reduces food intake or increases fat loss. Future developments of obesity therapeutics involve targeting multiple pathways. We hypothesised that NPY and dynorphin regulate energy homeostasis independently, thus double NPY and dynorphin ablation would result in greater weight and/or fat loss than the absence of NPY or dynorphin alone. Design and methodsWe generated single and double NPY and dynorphin knockout mice (NPYΔ, DYNΔ, NPYDYNΔ) and compared body weight, adiposity, feeding behaviour, glucose homeostasis and brown adipose tissue uncoupling protein-1 (UCP-1) expression to wildtype counterparts. Results Body weight and adiposity were significantly increased in NPYDYNΔ, but not in NPYΔ or DYNΔ. This was not due to increased food intake or altered UCP-1 expression, which were not significantly altered in double knockouts. NPYDYNΔ mice demonstrated increased body weight loss after a 24-h fast, with no effect on serum glucose levels after glucose injection. Conclusions Contrary to the predicted phenotype delineated from single knockouts, double NPY and dynorphin deletion resulted in heavier mice, with increased adiposity, despite no significant changes in food intake or UCP-1 activity. This indicates that combining long-term opioid antagonism with blockade of NPY-ergic systems may not produce anti-obesity effects.

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Feeding elicited by dynorphin (1–13) microinjections into the ventral tegmental area in rats

Cited by 61 publications

References 24 publications

Changes in mu-opioid receptor expression and function in the mesolimbic system after long-term access to a palatable diet

Changes in mu-opioid receptor expression and function in the mesolimbic system after long-term access to a palatable diet

kappa-Opioid receptor signaling and brain reward function

Double deletion of orexigenic neuropeptide Y and dynorphin results in paradoxical obesity in mice

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