Morphine enhances hedonic taste palatability in rats

Doyle, Timothy G.; Berridge, Kent; Gosnell, Blake A.

doi:10.1016/0091-3057(93)90572-b

Cited by 120 publications

(69 citation statements)

References 47 publications

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“…Opioid antagonists selectively reduce the consumption of a palatable food, while opioid agonists increase its consumption (Glass et al, 1999a;Gosnell et al, 1990). For example, morphine, an opioid agonist, increases the hedonic reactions elicited by sucrose in rats (Doyle et al, 1993). In line with these findings, consumption of palatable food modifies endogenous opioid levels in different areas of the brain (Dum et al, 1983;Kelley et al, 2003).…”

Section: Introductionmentioning

confidence: 69%

Differential Regulation of the Consummatory, Motivational and Anticipatory Aspects of Feeding Behavior by Dopaminergic and Opioidergic Drugs

Barbano

Cador

2005

Neuropsychopharmacol

114

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Various aspects of feeding behavior (eg consumption, motivation and anticipation) are regulated by homeostatic and hedonic systems, and are modulated by dopaminergic and opioid brain systems. Here, we have studied the modulation of these aspects of feeding behavior by opioid and dopaminergic neurotransmission while taking into account food palatability and homeostatic state. Foods that varied in palatability were presented to either food sated or food restricted rats following injections of different doses of naloxone, an opioid receptor antagonist, or flupenthixol, a dopaminergic receptor antagonist, in behavioral paradigms that measured different aspects of feeding. Naloxone decreased food intake in a dose-dependent manner in sated rats given access to palatable food, without modifying food intake in food restricted rats. Flupenthixol did not have any effect on food intake. With regard to motivation, which was tested in a straight alley, naloxone increased the latency to reach the food only in sated rats presented with palatable food. Flupenthixol did not modify the latency of any group. Conditioned locomotor activity to repeated food presentation, a measure of anticipation, is expressed only in food restricted rats. Naloxone did not modify anticipatory activity, whereas flupenthixol decreased it only in food restricted rats presented with palatable food. These results reinforce the idea that the opioid system regulates feeding through the modulation of the perceived palatability of food. The dopaminergic system seems to be more important for the regulation of anticipatory activity related to motivationally relevant stimuli.

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Section: Introductionmentioning

confidence: 69%

Differential Regulation of the Consummatory, Motivational and Anticipatory Aspects of Feeding Behavior by Dopaminergic and Opioidergic Drugs

Barbano

Cador

2005

Neuropsychopharmacol

114

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“…Food 'liking' is conveyed to the frontotemporal cortical structures (Berridge, 2003;Kelley, 2004b) through m-opioid neurotransmission within the scattered network of subcortical and brainstem nuclei (Tanda and Di Chiara, 1998;Saper et al, 2002;Berridge, 2003;Berridge and Robinson, 2003;Pecina et al, 2003;Berthoud, 2004b;Kelley, 2004b;, including the NAc, VTA, ventral pallidum, nucleus of the solitary tract, parabrachial nucleus, and the amygdala. Opioids enhance food pleasantness (Doyle et al, 1993;Pecina and Berridge, 1995;, whereas consumption of high-energy sweet and fat food increases endogenous opiates release (ie, feedforward interaction; Tanda and Di Chiara, 1998;Colantuoni et al, 2002;Grigson, 2002) so that analgesia (Mercer and Holder, 1997a;Segato et al, 1997;Lewkowski et al, 2003), opioid dependence (Schoenbaum et al, 1989(Schoenbaum et al, , 1990Colantuoni et al, 2001Colantuoni et al, , 2002, and compensatory decrease of opiate gene expression in the reward structures (Kelley et al, , 2005 may ensue.…”

Section: Neurobiology Of Systems Mediating Food Rewardmentioning

confidence: 99%

“…Furthermore, similarly to methadone-maintained patients (Willenbring et al, 1989;Zador et al, 1996), exaggerated opioidergic activity could enhance hedonic preference (ie, liking) for sweet and fatty foods (Doyle et al, 1993;Pecina and Berridge, 1995;. The consumption of these foods further reduces BDNF efficiency in preventing neuronal death (Molteni et al, 2002) and in regulating reward function (Horger et al, 1999;Kernie et al, 2000;Nakagawa et al, 2003), glucose metabolism (Tonra et al, 1999;Nakagawa et al, 2000;Ono et al, 2000), appetitive behaviors (Eisch et al, 2003;Itoh et al, 2004), and other important homeostatic processes (Xu et al, 2003).…”

Section: Abnormal Opioidergic Function May Impair Liking Processes Inmentioning

confidence: 99%

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Elman

Borsook

Lukas

2006

Neuropsychopharmacol

133

142

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Obesity is highly prevalent among patients with schizophrenia and is associated with detrimental health consequences. Although excessive consumption of fast food and pharmacotherapy with such second-generation antipsychotic agents (SGAs) as clozapine and olanzapine has been implicated in the schizophrenia/obesity comorbidity, the pathophysiology of this link remains unclear. Here, we propose a mechanism based on brain reward function, a relevant etiologic factor in both schizophrenia and overeating. A comprehensive literature search on neurobiology of schizophrenia and of eating behavior was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) energy homeostasis, (2) food reward and hedonics, (3) reward function in schizophrenia, and (4) metabolic effects of the SGAs. A mesolimbic hyperdopaminergic state may render motivational/incentive reward system insensitive to low salience/palatability food. This, together with poor cognitive control from hypofunctional prefrontal cortex and enhanced hedonic impact of food, owing to exaggerated opioidergic drive (clinically manifested as pain insensitivity), may underlie unhealthy eating habits in patients with schizophrenia. Treatment with SGAs purportedly improves dopamine-mediated reward aspects, but at the cost of increased appetite and worsened or at least not improved opiodergic capacity. These effects can further deteriorate eating patterns. Pathophysiological and therapeutic implications of these insights need further validation via prospective clinical trials and neuroimaging studies. INTRODUCTIONObesity has reached pandemic proportions and it is rapidly surpassing smoking as a number one killer in the industrialized world (Sturm, 2002;Skidmore and Yarnell, 2004). Its annual cost to the American society is staggering, and is estimated to be around $117 billion owing to related illnesses and loss of productivity (National Institute of Diabetes and Digestive and Kidney Diseases, 2005).In schizophrenia, obesity is twice as prevalent as in the general public, afflicting over half this patient population (Allison et al, 1999a;Dixon et al, 2000; American Diabetes Association, 2004;Marder et al, 2004;Wirshing, 2004). Besides negative psychosocial impacts (distorted selfesteem and societal stigmatization) and medications noncompliance, schizophrenics appear to be particularly susceptible to the detrimental medical sequelae of obesity such as the 'Metabolic Syndrome', which is a cluster of cardiovascular risk factors, including abdominal adiposity, insulin resistance, impaired, glucose tolerance, dyslipidemia, and hypertension (McKee et al, 1986;Mukherjee et al, 1996;Brown et al, 2000;Haupt and Newcomer, 2002;Ryan and Thakore, 2002;Ryan et al, 2003;Holt et al, 2004;Kohen, 2004;Marder et al, 2004;Lieberman et al, 2005).Excessive body weight gain (BWG) could be attributed to a constellation of endocrine, molecular, genetic, demographic, and lifestyle-related factors. Provided that a common tra...

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“…Acute challenge with low doses of nicotine (0.4 mg/kg, s.c) suppressed aversive reactions to quinine and enhanced positive reactions to sucrose, suggesting that in common with other abused drugs, nicotine enhances the affective evaluation of solutions [27][28][29][30][31]. In the same study, three weeks of repeated nicotine administration (twice daily injections progressively increased from 0.4-0.8 mg/kg, s.c) eliminated the ability of nicotine to modulate palatability, indicating tolerance to the effects of nicotine.…”

Section: Effects Of Nicotine Exposurementioning

confidence: 99%

“…To address this, we applied the measurement of taste reactivity as a probe of affective state, as previous studies suggest that taste reactivity patterns to palatable and unpalatable tastants reflect basal and ongoing "core" affective states [26]. For example, morphine and amphetamine, increase sucrose palatability [27,28] and suppress aversive taste reactions to the bitter tastant quinine [29][30][31], suggesting these drugs raise affective state in a manner akin to "reward". We analysed taste reactivity patterns to sucrose and quinine during continuous nicotine infusion and spontaneous withdrawal.…”

Section: Page 4 Of 33mentioning

confidence: 99%

Measurement of affective state during chronic nicotine treatment and withdrawal by affective taste reactivity in mice: The role of endocannabinoids

Wing¹,

Cagniard²,

Murphy³

et al. 2009

Biochemical Pharmacology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 of 33A c c e p t e d M a n u s c r i p t This work was funded by the RIKEN Brain Science Institute, and a BBSRC Japan Partnering Award. Page 2 of 33A c c e p t e d M a n u s c r i p t 2 AbstractDespite tobacco being highly addictive, it is unclear if nicotine has significant affective properties. To address this, we studied taste reactions to gustatory stimuli, palatable sucrose and unpalatable quinine, which are believed to reflect ongoing affective state. Taste reactivity was assessed during chronic nicotine administration and spontaneous withdrawal and the role of the endogenous cannabinoids was also investigated. C57BL6J mice were implanted with intra-oral fistula to allow passive administration of solutions. In the first study, taste reactivity was tracked throughout chronic vehicle or nicotine (12 mg/kg/day) infusion via osmotic minipumps and spontaneous withdrawal following removal of minipumps. In the second study, the endocannabinoid CB1 receptor antagonist AM251 (1, 3 and 10 mg/kg, intraperitoneal) or vehicle were acutely administered before taste reactivity measurement during chronic nicotine administration. Chronic nicotine treatment and spontaneous withdrawal did not influence taste reactions to sucrose or quinine. AM251 decreased positive reactions to sucrose and increased negative reactions to quinine. The effects of AM251 were respectively attenuated and enhanced in nicotine infused mice. These results suggest chronic nicotine exposure and withdrawal has no apparent affective sequelae, as probed by taste reactivity, and thus may not explain the difficulty tobacco-users have in achieving abstinence. In contrast, endocannabinoids elevates affective state in drug-naïve animals and changes in endogenous endocannabinoid tone may underlie compensations in affective state during chronic nicotine exposure.

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Morphine enhances hedonic taste palatability in rats

Cited by 120 publications

References 47 publications

Differential Regulation of the Consummatory, Motivational and Anticipatory Aspects of Feeding Behavior by Dopaminergic and Opioidergic Drugs

Differential Regulation of the Consummatory, Motivational and Anticipatory Aspects of Feeding Behavior by Dopaminergic and Opioidergic Drugs

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Measurement of affective state during chronic nicotine treatment and withdrawal by affective taste reactivity in mice: The role of endocannabinoids

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