Naloxone reduces amphetamine-induced stimulation of locomotor activity and in vivo dopamine release in the striatum and nucleus accumbens

Hooks, M.S.; Jones, Declan N.C.; Justice, Joseph B.; Holtzman, Stephen G.

doi:10.1016/0091-3057(92)90027-d

Cited by 58 publications

(28 citation statements)

References 25 publications

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“…This observation may be somewhat surprising since -opioid receptors are positioned to modulate mesolimbic and mesocortical DA transmission. Indeed, morphine activates both aforementioned DA projections (Di Chiara and Imperato, 1988;Devoto et al, 2002), and blocking -opioid receptors reduces amphetamine-induced increments in striatal DA release (Hooks et al, 1992;Schad et al, 1995). Furthermore, the current data with nor-BNI and naltrindole suggest that ␦-and -opioid receptors are not involved in (amphetamine-induced) impulsive choice.…”

Section: Opioids Amphetamine and Impulsive Choicementioning

confidence: 66%

“…Nonetheless, the current data extend previous data showing that acute challenges with psychostimulants such as amphetamine and cocaine activate endogenous opioid systems via DA-dependent mechanisms (Hurd and Herkenham, 1992;McGinty, 1995, 1996;Olive et al, 2001;RothDeri et al, 2003). Moreover, opioid receptors mediate the effects of amphetamine on DA release and behavioral measures including locomotion, reward, and amphetamineinduced reinstatement of amphetamine seeking (Trujillo et al, 1991;Hooks et al, 1992;Schad et al, 1995;JayaramLindström et al, 2004JayaramLindström et al, , 2008Häggkvist et al, 2009). Particularly the latter finding is of interest in view of the close interrelationship between impulsivity and relapse vulnerability (Perry and Carroll, 2008;Verdejo-García et al, 2008).…”

Section: Opioids Amphetamine and Inhibitory Controlmentioning

confidence: 95%

“…Thus, opioid receptor antagonists might be effective antirelapse agents because of their beneficial effects on impulsivity. Given the importance of (NAc) opioid systems in foodmotivated behavior (Kelley et al, 2002;Cota et al, 2006) and amphetamine-induced hyperlocomotion (Hooks et al, 1992;Schad et al, 1995;Gonzalez-Nicolini et al, 2003), it could be argued that the observed effects of opioid (ant)agonists on (amphetamine-induced) impulsivity might be related to direct effects on food motivated-behavior and/or somatomotor activity. However, this seems very unlikely since none of the tested compounds had clear effects on behavioral measures that could be interpreted as indices of motivation for food, namely errors of omission and feeder latencies.…”

Section: Opioids Amphetamine and Inhibitory Controlmentioning

confidence: 99%

“…Indeed, there is ample evidence showing that amphetamine activates endogenous opioid systems McGinty, 1995, 1996;Olive et al, 2001;Gonzalez-Nicolini et al, 2003), and the effects of amphetamine on DA release and behavioral measures including locomotion, reward, and amphetamine-induced rein-statement of amphetamine seeking involve opioid transmission (Trujillo et al, 1991;Hooks et al, 1992;Schad et al, 1995;Jayaram-Lindström et al, 2004Häggkvist et al, 2009). This raises the question as to whether endogenous opioids also mediate amphetamine-induced impulsivity.…”

Section: Introductionmentioning

confidence: 99%

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μ-Opioid Receptors in the Nucleus Accumbens Shell Region Mediate the Effects of Amphetamine on Inhibitory Control But Not Impulsive Choice

Wiskerke

Schetters

Es³

et al. 2011

J. Neurosci.

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Acute challenges with psychostimulants such as amphetamine affect impulsive behavior in both animals and humans. With regard to amphetamine, it is important to unravel how this drug affects impulsivity since it is not only a widely abused recreational drug but also regularly prescribed to ameliorate maladaptive impulsivity. Therefore, we studied the effects of amphetamine in two rat models of impulsivity, the five-choice serial reaction time task and the delayed-reward task, providing measures of inhibitory control and impulsive choice, respectively. We focused on the role of opioid receptor activation in amphetamine-induced impulsivity as there is ample evidence indicating an important role for endogenous opioids in several behavioral and neurochemical effects of amphetamine. Results showed that amphetamine-induced inhibitory control deficits were dose-dependently attenuated by the preferential -opioid receptor antagonist naloxone, but not by the selective ␦-opioid receptor antagonist naltrindole or -opioid receptor antagonist nor-BNI (norbinaltorphimine dihydrochloride). In contrast, naloxone did not affect amphetamine-induced improvements in impulsive decision making. Naloxone also completely prevented inhibitory control deficits induced by GBR -ol]-enkephalin acetate salt) revealed that -opioid receptor activation in the shell rather than the core subregion of the nucleus accumbens (NAc) modulates inhibitory control and subserves the effect of amphetamine thereon. Together, these results indicate an important role for NAc shell -opioid receptors in the regulation of inhibitory control, probably via an interaction between these receptors and the mesolimbic dopamine system.

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Section: Opioids Amphetamine and Impulsive Choicementioning

confidence: 66%

Section: Opioids Amphetamine and Inhibitory Controlmentioning

confidence: 95%

Section: Opioids Amphetamine and Inhibitory Controlmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

μ-Opioid Receptors in the Nucleus Accumbens Shell Region Mediate the Effects of Amphetamine on Inhibitory Control But Not Impulsive Choice

Wiskerke

Schetters

Es³

et al. 2011

J. Neurosci.

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show abstract

“…METH-induced conditioned place preference was found to be additively enhanced by co-administration with morphine [30], but inhibited by pretreatment with opioid receptor antagonist [49]. In various laboratory animal species, specific opioid receptor antagonist naloxone was found to decrease both AMPH-induced locomotor activity and AMPH-induced increase in extracellular levels of dopamine [12,41]. Moreover, morphine given alone not merely increases locomotor activity, but cross-sensitizes the behavioral effects to direct dopamine agonist, apomorphine, and indirect dopamine agonist, AMPH or METH [10,14,50].…”

Section: Introductionmentioning

confidence: 96%

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

Chiu

2005

Brain Research Bulletin

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Repeated intermittent exposure to psychostimulants was found to produce behavioral sensitization. The present study was designed to establish a mouse model and by which to investigate whether opioidergic system plays a role in methamphetamine-induced behavioral sensitization. Mice injected with 2.5 mg/kg of methamphetamine once a day for 7 consecutive days showed behavioral sensitization after challenge with 0.3125 mg/kg of the drug on day 11, whereas mice injected with a lower daily dose (1.25 mg/kg) did not. Mice received daily injections with either 1.25 or 2.5 mg/kg of methamphetamine showed behavioral sensitization after challenge with 1.25 mg/kg of the drug on days 11, 21, and 28. To investigate the role of opioidergic system in the induction and expression of behavioral sensitization, long-acting but non-selective opioid antagonist naltrexone was administrated prior to the daily injections of and challenge with methamphetamine, respectively. Our results show that the expressions of behavioral sensitization were attenuated by pretreatment with 10 or 20 mg/kg of naltrexone either during the induction period or before methamphetamine challenge when they were tested on days 11 and 21. These results indicate that repeated injection with methamphetamine dose-dependently induced behavioral sensitization in mice, and suggest the involvement of opioid receptors in the induction and expression of methamphetamine-induced behavioral sensitization.

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D1 and D2 receptor regulation of preproenkephalin and preprodynorphin mRNA in rat striatum following acute injection of amphetamine or methamphetamine

Wang

McGinty

1996

Synapse

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Our previous work has demonstrated a dose‐dependent induction of striatal preprodynorphin (PPD) in response to a single injection of the psychostimulants amphetamine (AMPH) or methamphetamine (METH). In the present study, dose‐response effects of acute administration of these stimulants on preproenkephalin (PPE) mRNA expression in the rat striatum were investigated with quantitative in situ hybridization histochemistry 3 h after injection. Acute AMPH or METH at equimolar doses (3.75, 7.5, 15, and 30 μmol/kg) significantly increased PPE mRNA expression in dorsal (caudoputamen), but not ventral (nucleus accumbens), striatum in a dose‐dependent fashion. In addition, the role of D1 and D2 dopamine receptors in mediating AMPH‐ and METH‐stimulated PPE and PPD expression was also evaluated by using subtype‐specific antagonists. Pretreatment of rats with SCH 23390 (0.1 mg/kg, i.p.), a selective D1 receptor antagonist, completely blocked acute AMPH (21 μmol/kg, i.p.)‐ or METH (21 μmol/kg, i.p.)‐induced PPE as well as PPD mRNA expression in the caudoputamen. Pretreatment with eticlopride (0.5 mg/kg, i.p.), a selective D2 receptor antagonist, also blocked PPD induction by the two stimulants, but PPE induction was unaffected. Furthermore, SCH 23390 decreased, and eticlopride elevated, constitutive PPE mRNA levels in the caudoputamen. Neither antagonist had a significant effect on the basal level of PPE or PPD mRNA in the nucleus accumbens. These results demonstrate a clear dose‐related responsiveness of PPE gene expression in striatal neurons in response to acute administration of amphetamines, although the intensity of the response is far less than that for striatal PPD. Furthermore, both D1 and D2 subtypes of dopamine receptors mediate AMPH‐ and METH‐stimulated striatal PPD mRNA expression, whereas D1 receptor activation alone mediates amphetamine‐stimulated PPE mRNA expression in the rat striatum. © 1996 Wiley‐Liss, Inc.

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Naloxone reduces amphetamine-induced stimulation of locomotor activity and in vivo dopamine release in the striatum and nucleus accumbens

Cited by 58 publications

References 25 publications

μ-Opioid Receptors in the Nucleus Accumbens Shell Region Mediate the Effects of Amphetamine on Inhibitory Control But Not Impulsive Choice

μ-Opioid Receptors in the Nucleus Accumbens Shell Region Mediate the Effects of Amphetamine on Inhibitory Control But Not Impulsive Choice

Attenuation of methamphetamine-induced behavioral sensitization in mice by systemic administration of naltrexone

D1 and D2 receptor regulation of preproenkephalin and preprodynorphin mRNA in rat striatum following acute injection of amphetamine or methamphetamine

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