Genetic and pharmacological manipulation of μ opioid receptors in mice reveals a differential effect on behavioral sensitization to cocaine

Hummel, Michele; Ansonoff, Micheal; Pintar, John E.; Unterwald, Ellen M.

doi:10.1016/j.neuroscience.2004.01.025

Cited by 36 publications

(35 citation statements)

References 64 publications

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“…For example, the motor stimulatory action of cocaine has been shown to be reduced in the presence of opioid receptor antagonists (Houdi et al 1989;Kim et al 1997) or in mice lacking the mu-opioid receptor (Hummel et al 2004). Importantly, cocaine has been reported to cause the release of beta-endorphin in the nucleus accumbens (Olive et al 2001), a response that could play a functional role in the motor stimulatory and rewarding actions of cocaine.…”

Section: Discussionmentioning

confidence: 99%

The role of beta-endorphin in the acute motor stimulatory and rewarding actions of cocaine in mice

et al. 2008

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Rationale-Opioid receptor antagonists have been shown to attenuate the rewarding and addictive effects of cocaine. Furthermore, cocaine has been shown to cause the release of beta-endorphin, an endogenous opioid peptide.Objective-We assessed whether this neuropeptide would play a functional role in cocaine-induced motor stimulation and conditioned place preference (CPP).Materials and methods-Mice lacking beta-endorphin and their wild-type littermates were habituated to motor activity chambers for 1 h, then injected with cocaine (0, 15, 30, or 60 mg/kg, intraperitoneally) or morphine (0, 5, or 10 mg/kg, subcutaneously), and motor activity was recorded for 1 h. In the CPP paradigm, mice were tested for baseline place preference on day 1. On days 2 and 3, mice received an alternate-day saline/cocaine (15, 30, or 60 mg/kg) or saline/ morphine (10 mg/kg) conditioning session and then tested for postconditioning place preference on day 4.Results-Cocaine-induced motor stimulation and CPP were both reduced in mice lacking betaendorphin. On the other hand, motor stimulation and CPP induced by morphine were not altered in mutant mice. Conclusion-The present results demonstrate that the endogenous opioid peptide beta-endorphin plays a modulatory role in the motor stimulatory and rewarding actions of acute cocaine.

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Section: Discussionmentioning

confidence: 99%

The role of beta-endorphin in the acute motor stimulatory and rewarding actions of cocaine in mice

et al. 2008

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“…Previous studies, including our own (Hummel et al 2004), have sought to establish a role for mu opioid receptors in acute cocaine-induced hyperlocomotion and sensitization using a murine mu opioid receptor knockout model. Results from these studies have been inconclusive.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, sensitization may model certain aspects of human addictive behaviors such as the intensification of drug craving (Robinson and Berridge 1993). Previous studies have demonstrated that nonselective opioid receptor antagonists can attenuate the development of sensitization to the locomotor-stimulating properties of cocaine (Kim et al 1997;Hummel et al 2004). Although data support the role of opioid receptors in cocaine-mediated locomotion and sensitization, the type of opioid receptor involved has not been established in the rat because of the previous use of nonselective opioid receptor antagonists.…”

Section: Introductionmentioning

confidence: 99%

A role for mu opioid receptors in cocaine-induced activity, sensitization, and reward in the rat

et al. 2007

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“…We did not observe a difference in cocaine-induced behavioral sensitization between CTOP and saline treated groups suggesting that in fact that m-opioid receptors are not required for behavioral sensitization to the locomotor stimulant effects of cocaine to develop, which is in agreement with the m-opioid receptor knockout experiment. In further support of a lack of involvement of m-opioid receptors in cocaine-induced behavioral sensitization, a recent study by Hummel et al (2004) reported cocaineinduced behavioral sensitization in exon 1 m-opioid receptor knockout mice. As mentioned, Yoo et al (2003) reported differential cocaine-induced behavioral sensitization in m-opioid receptor knockout mice.…”

Section: Cocaine-induced Behavioral Sensitizationmentioning

confidence: 90%

μ-Opioid Receptors are not Involved in Acute Cocaine-Induced Locomotor Activity nor in Development of Cocaine-Induced Behavioral Sensitization in Mice

Lesscher

Hordijk

Bondar

et al. 2004

Neuropsychopharmacol

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Although m-opioid receptors have been extensively investigated for their role in drug reinforcement, little is known about the contribution of these receptors to the acute and sensitized locomotor response to cocaine. In this study m-opioid receptor involvement in acute cocaine-induced locomotor activity and in the development of cocaine-induced behavioral sensitization was evaluated using mopioid receptor knockout mice and chronic naltrexone (NTX) pretreatment as models. In addition, co-administration of the specific mopioid receptor antagonist CTOP with repeated saline or cocaine injections was used to establish the involvement of m-opioid receptors in sensitization to the locomotor stimulant effects of cocaine. The acute locomotor response to cocaine (3, 10, 20, or 30 mg/kg i.p.) of mopioid receptor knockout or chronic NTX pretreated mice was not different from the cocaine response of their respective controls. With respect to cocaine-induced behavioral sensitization, induced by daily injections of 20 mg/kg cocaine for 11 subsequent days, mopioid receptor knockout mice developed behavioral sensitization to the locomotor stimulant effects of cocaine (challenge 10 mg/kg i.p.) comparable to wild-type littermates and the m-opioid receptor antagonist CTOP did not affect cocaine-induced sensitization either. However, mice that were pretreated with NTX exhibited augmented cocaine-induced behavioral sensitization relative to placebo pretreated controls, which may be ascribed to increased d-opioid receptor levels as has been described for chronic NTX pretreated mice. The present findings suggest that m-opioid receptors are not required for the acute locomotor response to cocaine nor are they essential for the development of cocaine-induced behavioral sensitization.

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Genetic and pharmacological manipulation of μ opioid receptors in mice reveals a differential effect on behavioral sensitization to cocaine

Cited by 36 publications

References 64 publications

The role of beta-endorphin in the acute motor stimulatory and rewarding actions of cocaine in mice

The role of beta-endorphin in the acute motor stimulatory and rewarding actions of cocaine in mice

A role for mu opioid receptors in cocaine-induced activity, sensitization, and reward in the rat

μ-Opioid Receptors are not Involved in Acute Cocaine-Induced Locomotor Activity nor in Development of Cocaine-Induced Behavioral Sensitization in Mice

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