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

Cunningham, Christopher L.; Dickinson, Shelly D.; Okorn, Dobrina M.

doi:10.1037/1064-1297.3.4.330

Cited by 53 publications

(54 citation statements)

References 70 publications

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“…Cunningham et al (1995) found no effect of naloxone pretreatment on ethanol-induced locomotor stimulation in DBA/2J mice. This study assessed locomotor activity during the first 5-min period after ethanol administration (2 g/kg), the time when pure stimulation (with no sedation) is most likely to be seen (Shen et al 1995).…”

Section: Discussionmentioning

confidence: 87%

“…In clinical studies (King et al 1997;Swift et al 1994), naltrexone attenuated ethanol-induced increases in stimulation scores as measured by the Biphasic Alcohol Effects Scale. In addition, naltrexone and another nonspecific opioid receptor antagonist, naloxone, which both attenuate morphine-induced locomotor stimulation (Powell and Holtzman 2001;Sanchis-Segura et al 2004), were found to attenuate ethanol-induced locomotor stimulation without affecting baseline activity levels in several inbred (BALB/cJ, DBA/2J) and outbred (CD-1, Swiss) strains of mice (Camarini et al 2000;Kiianmaa et al 1983;Pastor et al 2005;SanchisSegura et al 2004; but see Cunningham et al 1995;Gevaerd et al 1999). Naltrexone did not attenuate ethanolinduced locomotor depression, however, in C57BL/6J mice (Middaugh et al 1978).…”

Section: Introductionmentioning

confidence: 92%

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Naloxone does not attenuate the locomotor effects of ethanol in FAST, SLOW, or two heterogeneous stocks of mice

et al. 2005

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Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 92%

Naloxone does not attenuate the locomotor effects of ethanol in FAST, SLOW, or two heterogeneous stocks of mice

et al. 2005

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“…The possibility of a dissociation between the mechanisms underlying primary and conditioned reinforcing effects induced by ethanol is an important consideration in the evaluation of pharmacotherapies and other manipulations that influence alcohol-seeking behavior (cf. Cunningham et al 1995).…”

Section: Discussionmentioning

confidence: 95%

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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“…Given previous evidence of naloxone's ability to induce a conditioned place aversion in mice (e.g., Mucha and Walker 1987;Cunningham et al 1995) and the finding that repeated testing with naloxone converted place preference to place aversion, one must consider the possibility that test session exposures to naloxone actually conditioned an aversion to the CS previously paired with ethanol. One problem with this suggestion is that mice were exposed to both CS+ and CS-in the presence of naloxone during the test.…”

Section: Figmentioning

confidence: 99%

Extinction of ethanol-induced conditioned place preference and conditioned place aversion: effects of naloxone

1998

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Four experiments examined the effect of naloxone pretreatment on the expression and extinction of ethanol-induced conditioned place preference (experiments 1, 2, 4) or conditioned place aversion (experiments 1, 3). DBA/2 J mice received four pairings of a distinctive tactile (floor) stimulus (CS) with injection of ethanol (2 g/kg) given either immediately before or after 5-min exposure to the CS. A different stimulus was paired with injection of saline. Pre-CS injection of ethanol produced conditioned place preference, whereas post-CS injection of ethanol produced conditioned place aversion. Both behaviors extinguished partially during repeated choice testing after vehicle injection. Naloxone (10 mg/kg) had little effect on the initial expression of conditioned place preference, but facilitated its extinction. Moreover, repeated naloxone testing resulted in the expression of a weak conditioned place aversion to the CS that initially elicited a place preference. In contrast, naloxone (1.5 or 10 mg/kg) enhanced expression of conditioned place aversion, thereby increasing its resistance to extinction. A control experiment (experiment 4) indicated that repeated testing with a different aversive drug, lithium chloride, did not affect rate of extinction or produce an aversion to the CS previously paired with ethanol. These findings do not support the suggestion that naloxone facilitates the general processes that underlie extinction of associative learning. Also, these data are not readily explained by the conditioning of place aversion at the time of testing. Rather, naloxone's effects appear to reflect a selective influence on maintenance of ethanol's conditioned rewarding effect, an effect that may be mediated by release of endogenous opioids. Overall, these findings encourage further consideration of the use of opiate antagonists in the treatment of alcoholism.

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

Cited by 53 publications

References 70 publications

Naloxone does not attenuate the locomotor effects of ethanol in FAST, SLOW, or two heterogeneous stocks of mice

Naloxone does not attenuate the locomotor effects of ethanol in FAST, SLOW, or two heterogeneous stocks of mice

Flavor preference conditioning by oral self-administration of ethanol

Extinction of ethanol-induced conditioned place preference and conditioned place aversion: effects of naloxone

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