Dietary Modulation Of Mu And Kappa Opioid Receptor-mediated Analgesia

Kanarek, Robin B.; Przypek, Jeanne; D’Anci, Kristen E.; Marks-Kaufman, Robin

doi:10.1016/s0091-3057(96)00470-4

Cited by 42 publications

(22 citation statements)

References 45 publications

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“…*Indicates that %MPEs were significantly greater ð p , 0:05Þ for rats given sucrose to drink vs. rats given only chow and water. with our previous research (Kanarek et al, 1991;Frye et al, 1993;D'Anci et al, 1996;D'Anci et al, 1997;Kanarek et al, 1997b;D'Anci, 1999). Additionally, the present experiment extends these findings to a warm-water tail-withdrawal procedure, and the data are comparable to the radiant-heat tail-flick procedure.…”

supporting

confidence: 89%

“…Keywords: Antinociception; Long-Evans; Morphine; Naltrexone; Rats; Sucrose It is well documented that long-term intake of palatable, nutritive fluids increases sensitivity to the analgesic properties of morphine (Schoenbaum et al, 1989;Roane and Martin, 1990;Kanarek et al, 1991Kanarek et al, , 1997bFrye et al, 1992;D'Anci et al, 1996D'Anci et al, , 1997Nikfar et al, 1997Nikfar et al, , 1998D'Anci, 1999). Additionally, we have previously shown that prior intake of highly palatable fluids increases the ability of naltrexone to decrease intake of standard rodent chow (Kanarek et al, 1997a).…”

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confidence: 99%

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D’Anci

Kanarek²

2004

Nutritional Neuroscience

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Rats given long-term access to a palatable sucrose solution are more sensitive to (1) the analgesic potency of morphine and (2) the anorectic actions of naltrexone. In the present experiment, the ability of naltrexone to antagonize the antinociceptive properties of morphine was examined in sucrose- and chow-fed rats. Twenty adult male Long-Evans rats were maintained on chow and water. Ten rats were also given ad libitum access to a 32% sucrose solution for three weeks. Baseline and post-drug nociceptive thresholds were determined with a warm water (52 degrees C) tail-withdrawal procedure. Complete morphine dose-effect curves (0.32-100.0 mg/kg) were determined alone and in the presence of naltrexone (0.32-0.32 mg/kg). Morphine produced significant increases in tail-withdrawal latencies in both groups of animals. Rats drinking sucrose had significantly longer tail-withdrawal latencies than rats given only chow and water. Naltrexone produced significant and surmountable dose-dependent rightward shifts in the morphine dose-response curves for both groups, but did not differ in potency across diets. The present data support and extend our earlier findings showing sucrose enhancement of morphine-induced antinociception in rats given a palatable sucrose solution to drink.

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confidence: 89%

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confidence: 99%

Short Communication

D’Anci

Kanarek²

2004

Nutritional Neuroscience

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“…Also, naloxone at doses that do not block place preference for sucrose decreases sucrose consumption, suggesting that the rewarding properties (i.e., hedonic properties) of sucrose are more sensitive to the antagonist effects than its reinforcing properties (Agmo et al 1995). In the same way, it has been demonstrated that opioid-like analgesia can be generated by the ingestion of a sweet solution or fat, and this ingestion also potentiates the analgesic effects of morphine (Bergmann et al 1985;Kanarek et al 1997).…”

Section: Dopamine and Food Anticipationmentioning

confidence: 98%

Opioids for hedonic experience and dopamine to get ready for it

2006

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Altogether, the data presented point out for an implication of dopamine in the anticipatory/preparatory aspects of feeding more than on the motivational and consummatory aspects. However, dopamine involvement in the anticipatory/preparatory component of feeding seems specifically related to very relevant stimuli, such as highly palatable foods. On the other hand, our data, as well as those present in the literature, strongly suggest a role for opioids in food intake through their modulation of the hedonic perception of food. As a consequence, opioids are involved in those aspects of motivation driven by food palatability rather than by food homeostatic need.

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“…It is interesting to speculate that this system may be responsible for the effect that "comfort foods" have on mood and general emotional state in humans. Supportive of this notion is the finding that in humans and animals, consumption of high fat or sweet foods has been shown to induce analgesia (Kanarek et al, 1997), suggesting that their consumption can literally alter the perception of pain. Consumption of chocolate or sugar activates brain circuits encoding emotion and increases pleasurable feelings (Small et al, 2001).…”

Section: Opioids and Palatabilitymentioning

confidence: 99%

A proposed hypothalamic–thalamic–striatal axis for the integration of energy balance, arousal, and food reward

Kelley

Baldo

Pratt

2005

J of Comparative Neurology

313

286

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We elaborate herein a novel theory of basal ganglia function that accounts for why palatable, energy-dense foods retain high incentive value even when immediate physiological energy requirements have been met. Basal ganglia function has been studied from the perspective of topographical segregation of processing within parallel circuits, with primary focus on motor control and cognition. Recent findings suggest, however, that the striatum can act as an integrated unit to modulate motivational state. We describe evidence that the striatal enkephalin system, which regulates the hedonic impact of preferred foods, undergoes coordinated gene expression changes that track current motivational state with regard to food intake. Striatal enkephalin gene expression is also downregulated by an intrastriatal infusion of a cholinergic muscarinic antagonist, a manipulation that greatly suppresses food intake. To account for these findings, we propose that signaling through a hypothalamic-midline thalamic-striatal axis impinges on the cholinergic interneurons of the striatum, which via their large, overlapping axonal fields act as a network to modulate enkephalin-containing striatal output neurons. A key relay in this circuit is the paraventricular thalamic nucleus, which receives convergent input from orexin-coded hypothalamic energy-sensing and behavioral state-regulating neurons, as well as from circadian oscillators, and projects to cholinergic interneurons throughout the striatal complex. We hypothesize that this system evolved to coordinate feeding and arousal, and to prolong the feeding central motivational state beyond the fulfillment of acute energy needs, thereby promoting "overeating" and the consequent development of an energy reserve for potential future food shortages.

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Dietary Modulation Of Mu And Kappa Opioid Receptor-mediated Analgesia

Cited by 42 publications

References 45 publications

Short Communication

Short Communication

Opioids for hedonic experience and dopamine to get ready for it

A proposed hypothalamic–thalamic–striatal axis for the integration of energy balance, arousal, and food reward

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