Cocaine place preference is blocked by the δ-opioid receptor antagonist, naltrindole

Menkens, Kent A.; Bilsky, Edward J.; Wild, Kenneth D.; Portoghese, Philip S.; Reid, Larry D.; Porreca, Frank

doi:10.1016/0014-2999(92)90319-y

Cited by 106 publications

(42 citation statements)

References 2 publications

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“…Effects of endogenous enkephalins acting at delta opioid receptors in intact systems have been demonstrated to contribute to stimulant-mediated behaviors (Jones and Holtzman, 1992;Menkens et al, 1992) and dopamine release (Schad et al, 1996). However, in the present study NTI had no effect alone on amphetamine-mediated dopamine efflux, probably indicating a lack of endogenous enkephalinergic tone in isolated striatal tissue.…”

Section: Discussioncontrasting

confidence: 66%

The selective delta opioid agonist SNC80 enhances amphetamine-mediated efflux of dopamine from rat striatum

et al. 2008

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The highly selective delta opioid agonist, SNC80, elicits dopamine-related behaviors including locomotor stimulation and conditioned place-preference. In contrast, it has been reported that SNC80 fails to promote dopamine efflux from the striatum of freely moving rats. However, SNC80 does enhance behavioral responses to the stimulants, amphetamine and cocaine, suggesting an interaction between delta opioids and psychostimulants. Since the increase in locomotor activity elicited by amphetamine and related stimulants acting at the dopamine transporter is associated with increases in extracellular concentrations of dopamine within the striatum, we hypothesized that SNC80 enhances this activity by potentiating the overflow of dopamine through the transporter. To test this hypothesis, striatal preparations from Sprague-Dawley rats were assayed for dopamine efflux in response to amphetamine challenge. SNC80 was given either in vivo or in vitro directly to rat striatal tissue, prior to in vitro amphetamine challenge. Both in vivo and in vitro administration of SNC80 enhanced amphetamine-mediated dopamine efflux in a concentration-and time-dependent manner. However, SNC80 in either treatment paradigm produced no stimulation of dopamine efflux in the absence of amphetamine. The effect of SNC80 on amphetamine-mediated dopamine overflow, but not the effect of amphetamine alone, was blocked by the delta selective antagonist, naltrindole and was also observed with other delta agonists. The results of this study demonstrate that even though SNC80 does not stimulate dopamine efflux alone, it is able to augment amphetamine-mediated dopamine efflux through a delta opioid receptor mediated action locally in the striatum.

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Section: Discussioncontrasting

confidence: 66%

The selective delta opioid agonist SNC80 enhances amphetamine-mediated efflux of dopamine from rat striatum

et al. 2008

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“…Therefore, these findings suggest partial involvement of 6-opioid receptors in psychic dependence on morphine. Indeed, pretreatment with 6-opioid antagonists is capable of abolishing the reinforcing properties of morphine (unpublished observation) and cocaine (Menkens et al 1992) To summarize, the activation of NTI-and NTBsensitive 6-opioid receptors plays a partial role in the morphine-induced hyperlocomotion and enhancement of DA turnover in the limbic forebrain, but not antinociception in mice.…”

Section: Discussionmentioning

confidence: 94%

Involvement of δ-opioid receptors in the effects of morphine on locomotor activity and the mesolimbic dopaminergic system in mice

et al. 1993

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Naltrindole (NTI) and naltriben (NTB), a benzofuran derivative of NTI, were recently synthesized as highly selective delta-opioid receptor antagonists. Both NTI and NTB failed to suppress the antinociceptive effect induced by morphine. In contrast, both NTI and NTB significantly suppressed the morphine-induced hyperlocomotion and increase in turnover of dopamine (DA) in the mouse limbic forebrain. These results suggest that delta-opioid receptors play, at least in part, a role in the morphine-induced hyperlocomotion and excitation of mesolimbic DA systems, but not antinociception.

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“…Anatomical and neurochemical evidence support the interaction between the opioidergic and dopaminergic systems within the motive circuit (Di Chiara and Imperato, 1988;Devine et al, 1993;Churchill and Kalivas, 1996;Feigenbaum and Howard, 1997;Svingos et al, 1996Svingos et al, , 1998Svingos et al, , 1999Svingos et al, , 2001Garzon and Pickel, 2001). In addition, in several different animal models of drug reinforcement, opioid receptor antagonists have been shown to attenuate the rewarding effects of psychostimulants (Menkens et al, 1992;Sala et al, 1995;Kuzmin et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Expression of Amphetamine-Induced Behavioral Sensitization after Short- and Long-Term Withdrawal Periods: Participation of μ- and δ-Opioid Receptors

Magendzo

Bustos

2002

Neuropsychopharmacol

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Repeated amphetamine administration results in behavioral sensitization, an enduring behavioral transformation expressed after short and long periods of withdrawal. To investigate the participation of the opioid system in amphetamine-induced behavioral sensitization, we studied the effect of naloxone, an opioid receptor antagonist, on the expression of behavioral sensitization tested after short-(2 days) and long-term (14 days) withdrawal periods. In addition, using quantitative competitive RT-PCR, we examined the levels of m-opioid receptor (MOR) and d-opioid receptor (DOR) mRNA in the nucleus accumbens shell (NAcSh) and ventral tegmental area (VTA) of behaviorally sensitized rats, at these two withdrawal times. This study showed that whereas naloxone did not modify the expression of behavioral sensitization tested after 2 days of withdrawal, it completely blocked the expression when tested after 14 days of withdrawal. DOR and MOR mRNA levels were not modified in the NAcSh of rats expressing behavioral sensitization after 2 or 14 days of withdrawal. Conversely, DOR and MOR mRNA levels were elevated in the VTA of animals expressing behavioral sensitization after 2 days of withdrawal. However, whereas DOR mRNA returned to control levels, MOR mRNA levels remained elevated in animals expressing behavioral sensitization after 14 days of withdrawal. These results indicate a striking difference between the role played by opioid receptors in the expression of amphetamine-induced behavioral sensitization, when tested after short-or long-term withdrawal periods. In addition, our results support the notion that repeated amphetamine-induced changes in opioid receptor expression may contribute to the perpetuation of psychostimulant abuse and/or relapse.

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Cocaine place preference is blocked by the δ-opioid receptor antagonist, naltrindole

Cited by 106 publications

References 2 publications

The selective delta opioid agonist SNC80 enhances amphetamine-mediated efflux of dopamine from rat striatum

The selective delta opioid agonist SNC80 enhances amphetamine-mediated efflux of dopamine from rat striatum

Involvement of δ-opioid receptors in the effects of morphine on locomotor activity and the mesolimbic dopaminergic system in mice

Expression of Amphetamine-Induced Behavioral Sensitization after Short- and Long-Term Withdrawal Periods: Participation of μ- and δ-Opioid Receptors

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