Non-specific enhancement of ethanol-induced taste aversion by naloxone

Miceli, D.; Marfaing-Jallat, P.; Magnen, J. Le

doi:10.1016/0091-3057(79)90113-8

Cited by 23 publications

(9 citation statements)

References 27 publications

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“…A connection between opioids and oxytocin in other aspects of ingestive behavior has also been shown. For example, opiates reduce taste aversion and accompanying oxytocin neuronal activation [31], whereas antagonism of opioid receptors potentiates taste aversions [22] and oxytocin cellular activity induced by other agents and, by itself, can lead to aversion as well. Finally, other functional and neuroanatomical data point to the opioid-oxytocin system relationship.…”

Section: Discussionmentioning

confidence: 99%

Chronic sugar intake dampens feeding-related activity of neurons synthesizing a satiety mediator, oxytocin

et al. 2010

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Increased tone of orexigens mediating reward occurs upon repeated consumption of sweet foods. Interestingly, some of these reward orexigens, such as opioids, diminish activity of neurons synthesizing oxytocin, a nonapeptide that promotes satiety and feeding termination. It is not known, however, whether consumption-related activity of the central oxytocin system is modified under chronic sugar feeding reward itself. Therefore, we examined how chronic consumption of a rewarding high-sucrose (HS) vs. bland cornstarch (CS) diet affected the activity of oxytocin cells in the hypothalamus at the time of meal termination. Schedule-fed (2 hrs/day) rats received either a HS or CS powdered diet for 20 days. On the 21st day, they were given the same or the opposite diet, and food was removed after the main consummatory activity was completed. Animals were perfused 60 minutes after feeding termination and brains were immunostained for oxytocin and the marker of neuronal activity, c-Fos. The percentage of c-Fos-positive oxytocin cells in the hypothalamic paraventricular nucleus was significantly lower in rats chronically exposed to the HS than to the CS diet, regardless of which diet they received on the final day. A similar pattern was observed in the supraoptic nucleus. We conclude that the chronic rather than acute sucrose intake reduces activity of the anorexigenic oxytocin system. These findings indicate that chronic consumption of sugar blunts activity of pathways that mediate satiety. We speculate that a reduction in central satiety signaling precipitated by regular intake of foods high in sugar may lead to generalized overeating.

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Section: Discussionmentioning

confidence: 99%

Chronic sugar intake dampens feeding-related activity of neurons synthesizing a satiety mediator, oxytocin

et al. 2010

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“…Many studies have shown that rats will learn to avoid flavor solutions that have been paired with injection or rapid ingestion of ethanol (e.g., Lester et al 1970;Cappell et al 1973;Berman and Cannon 1974;Eckardt et al 1974;Eckardt 1975aEckardt ,b, 1976Cannon et al 1977; Barker and Johns 1978;Cunningham 1979;Linakis and Cunningham, 1979;Marfaing-Jallat and LeMagnen 1979;Miceli et al 1979). The development of such conditioned aversions appears to be at odds with the frequently reported finding that self-administered ethanol serves as a positive reinforcer for rats in operant tasks (e.g., Meisch and Thompson 1974a,b;Meisch 1977;Samson and Pfeffer 1987;Samson et al 1988).…”

Section: Introductionmentioning

confidence: 98%

Flavor preference conditioning by oral self-administration of ethanol

Cunningham

Niehus

1997

Psychopharmacology

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Oral self-administration and operant tasks have been used successfully to confirm ethanol's positive reinforcing effects in rats. However, in flavor conditioning tasks, ethanol is typically found to have aversive effects. The present studies explored this apparent paradox by examining the change in value of a flavor paired with orally self-administered ethanol in two different limited-access procedures. Rats were food-deprived and trained to drink (experiment 1) or to barpress for (experiment 2) 10% (v/v) ethanol during daily 30-min sessions using prandial initiation techniques. All rats were then exposed to a differential flavor conditioning procedure in which banana or almond extract was added to the drinking solution. One flavor (counterbalanced) was always mixed with ethanol (CS+), whereas the other flavor was mixed with water (CS-). By the end of conditioning, rats in both experiments drank more flavored ethanol than flavored water, confirming ethanol's efficacy as a reinforcer. Moreover, barpress rates for CS+ exceeded those for CS- in the operant task. Ethanol doses self-administered in final sessions averaged about 1 g/kg. The effect of the flavor-ethanol contingency was assessed in preference tests that offered a choice between the two flavor solutions without ethanol. In both experiments, subjects developed a preference for the flavor that had been paired with ethanol. Thus, the outcome of flavor conditioning was consistent with that of the oral self-administration tasks in providing evidence of ethanol's rewarding effects. These experiments confirm and extend previous studies showing that flavor aversion is not the inevitable result of flavor-ethanol association in rats. It seems likely that ethanol's nutrient and pharmacological effects both contributed to the development of conditioned flavor preference.

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“…Additional evidence of a possible opioid influence on ethanol's subjective effects is provided by the finding that naloxone interferes with the discriminative stimulus produced during the initial, excitatory phase of ethanol's effects but does not alter the stimulus produced during the later, sedative phase effects (Shippenberg & Altshuler, 1985). Furthermore, the opioid system has been implicated in ethanol's aversive effects by studies showing opiate antagonist effects on ethanol-induced conditioned taste aversion, although the direction of this effect has varied across studies (Miceli, Marfaing-Jallat, & Le Magnen, 1979; Ng Cheong Ton & Amit, 1984). Finally, there is evidence from studies of inbred mice and selectively bred rats suggesting that ethanol drinking and preference are genetically correlated with opioid system differences (Froehlich, 1993; Gianoulakis & de Waele, 1994).…”

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Naloxone facilitates extinction but does not affect acquisition or expression of ethanol-induced conditioned place preference.

Cunningham¹,

Dickinson

Okorn

1995

Experimental and Clinical Psychopharmacology

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Mice (DBA/2J) received a Pavlovian procedure in which a distinctive floor stimulus was paired 4 times with ethanol (2 g/kg). A different floor stimulus was paired with saline. Naloxone (0.0,1.5, or 10.0 mg/kg, intraperitoneal) given before each ethanol trial did not interfere with acquisition of conditioned preference, although naloxone alone produced conditioned aversion. When naloxone (0.0, 0.15, 1.5, 3.0, or 10.0 mg/kg) was given for the first time during testing, mice showed conditioned preference during the first 10 min. However, preference subsequently decreased dose-dependently over time. Control studies eliminated alternative interpretations based on pharmacokinetics or presence of an aversive state. The overall pattern of results suggests that naloxone facilitated extinction of conditioned place preference and supports the hypothesis that ethanol-induced conditioned reinforcement is mediated by the endogenous opioid system.Opioid system involvement in the hedonic (i.e., rewarding or aversive) effects of ethanol has been suggested by several different kinds of findings. Foremost among these findings are studies showing a suppressive effect of opiate antagonists on ethanol drinking or on operant responding for ethanol (e.g.,

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Non-specific enhancement of ethanol-induced taste aversion by naloxone

Cited by 23 publications

References 27 publications

Chronic sugar intake dampens feeding-related activity of neurons synthesizing a satiety mediator, oxytocin

Chronic sugar intake dampens feeding-related activity of neurons synthesizing a satiety mediator, oxytocin

Flavor preference conditioning by oral self-administration of ethanol

Naloxone facilitates extinction but does not affect acquisition or expression of ethanol-induced conditioned place preference.

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