Attenuation of ethanol-induced conditioned taste aversion by naloxazone: Behavioral evidence for an opiate receptor-mediated morphine-ethanol interaction

Ton, J.M. Ng Cheong; Amit, Zalman

doi:10.1016/0304-3940(84)90007-7

Cited by 14 publications

(2 citation statements)

References 23 publications

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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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confidence: 99%

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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confidence: 99%

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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“…The contrasting effects of naltrexone on the CTAs of ob/ob and lean mice in this study mirror the complex, and sometimes paradoxical, findings of others who have examined the role of opiates in CTA formation. In rats, CTAs have been produced (without LiCl) by following ingestion with an injection of either morphine (Mucha & Herz, 1985; Ng Cheong Ton & Amit, 1984) or one of several opiate antagonists (Pilcher, Stolerman, & D'Mello, 1978; Stolerman, Pilcher, & D'Mello, 1978). In the present study, 10 mg/kg naltrexone did not, by itself, influence saccharin preferences in either ob/ob or lean mice.…”

Section: Methodsmentioning

confidence: 99%

Propensity to form conditioned taste aversions augments anorexia in obese (Ob/Ob) mice with B16 melanoma.

Thompson¹,

Margules²,

Kreider³

et al. 1993

Behavioral Neuroscience

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Ob/ob mice (OB) with B16 melanoma become anorectic, but lean mice (LN) do not. Present studies suggest that this difference reflects a greater bent for OB to form conditioned taste aversions (CTA). In Exp 1, healthy OB formed stronger CTAs than LN to a saccharin taste paired with lithium chloride (LiCl, 3 mEq/kg ip). In Exp 2, the OB-LN difference of Exp 1 was decreased by giving naltrexone (10 mg/kg sc) before LiCl, which suggested opiate involvement. Exp 3 showed that OB tumor anorexia vanishes if foods dissociated from tumor growth are given: OB fed a constant diet became anorectic 16 days after B16 inoculation; giving a new diet on Day 16 delayed anorexia onset for 8 days; a second new diet on Day 32 abolished anorexia for 24 hr. LN with tumors ate all diets at nontumor control levels. OB survived melanoma longer than LN regardless of diet, but OB fed a varied diet died first; thus, anorexia may enhance OB survival.

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Narcotic antagonism of seizures induced by a dopamine-derived tetrahydroisoquinoline alkaloid

Blum

1988

Experientia

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This paper describes experiments designed to evaluate whether the narcotic antagonist naloxone significantly interferes with seizures induced by tetrahydroisoquinolines (TIQs). In these experiments we found that naloxone significantly reduced seizure scores induced by intra-cranially infusing mice with 50 micrograms of the dopamine-derived tetrahydroisoquinoline (TIQ) alkaloid, 6,7-dihydroxy TIQ. These findings support an opioid involvement in the actions of TIQs and may lead to further understanding of opioid-mediated novel excitatory receptors.

show abstract

Attenuation of ethanol-induced conditioned taste aversion by naloxazone: Behavioral evidence for an opiate receptor-mediated morphine-ethanol interaction

Cited by 14 publications

References 23 publications

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

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

Propensity to form conditioned taste aversions augments anorexia in obese (Ob/Ob) mice with B16 melanoma.

Narcotic antagonism of seizures induced by a dopamine-derived tetrahydroisoquinoline alkaloid

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