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

Magendzo, Karin; Bustos, Gonzalo

doi:10.1038/sj.npp.1300063

Cited by 34 publications

(32 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A previous study in rats, which was similar to this experiment, found that naloxone (5 mg/kg) did not modify the expression of behavioral sensitization after 2 days of abstinence, but it completely blocked the expression when tested after 14 days of abstinence [27]. Although the inhibitory effects of 10 and 20 mg/kg of NAT on day 21 appeared to be more potent than those on day 11, the discrepancies may have resulted from differences in subjects, drugs, or experimental conditions used in the two studies.…”

Section: Discussionsupporting

confidence: 79%

“…This up-regulation of opioid receptors has been shown to accompany supersensitivity to opioid agonists and is an indication of their functional relevance [48]. Moreover, repeated treatment with AMPH or METH was found to increase not only the mRNA levels of μ-opioid receptors in the VTA and NAcc [27] but also the dopamine releasing effects of μ-opioid receptor agonist [55]. This suggested that the alterations in μ-opioid receptors are functionally involved.…”

Section: Discussionmentioning

confidence: 82%

See 1 more Smart Citation

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

Chiu

2005

Brain Research Bulletin

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 82%

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

Chiu

2005

Brain Research Bulletin

View full text Add to dashboard Cite

show abstract

“…However, inherent to application of classic knockout strategies and hence lack of a specific gene from gestation, the possibility that for example d-opioid receptors have compensated for the loss of m-opioid receptors in this case cannot be ruled out. Retained cocaine-induced behavioral sensitization for m-opioid receptor knockout mice is not in agreement with previous studies, which suggested a role of m-opioid receptors in psychostimulant sensitization (Sala et al, 1995;Magendzo and Bustos, 2003;Yoo et al, 2003). Therefore, a subsequent experiment was performed to elucidate the role of m-opioid receptors in cocaine-induced sensitization.…”

Section: Cocaine-induced Behavioral Sensitizationsupporting

confidence: 45%

“…A role of m-opioid receptors in psychostimulant sensitization was suggested first of all by impaired cocaineinduced sensitization after NTX co-administered with cocaine (Sala et al, 1995) and also by findings of two recent studies. Expression of mRNA encoding m-and d-opioid receptors was increased in the VTA of amphetaminesensitized rats (Magendzo and Bustos, 2003). Another study dealt with cocaine-induced behavioral sensitization in mice with a targeted deletion of exons 2 and 3 of the m-opioid receptor gene.…”

Section: Cocaine-induced Behavioral Sensitizationmentioning

confidence: 99%

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

View full text Add to dashboard Cite

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.

show abstract

“…Doudet and Holden (2003) also reported that MA competed for the same D2 receptors as the dopamine antagonist, raclopride. Magendzo and Bustos (2003) demonstrated in rats that acute MA exposure resulted in increased transcription of mu opioid receptor and delta opioid receptor in the ventral tegmental area, which corresponded with an acute sensitization to MA. These results implicate the indirect striatopallidal pathway because of the colocalization of enkephalin (via the mu receptor) and GABA.…”

Section: Motor Dysfunction Following Ma Preclinical Studiesmentioning

confidence: 97%

Do Preclinical Findings of Methamphetamine-Induced Motor Abnormalities Translate to an Observable Clinical Phenotype?

Caligiuri

Buitenhuys

2005

Neuropsychopharmacol

View full text Add to dashboard Cite

This review summarizes the preclinical literature of the effects of methamphetamine (MA) on subcortical dopaminergic and GABAergic mechanisms underlying motor behavior with the goal of elucidating the clinical presentation of human MA-induced movement disorders. Acute and chronic MA exposure in laboratory animal can lead to a variety of motor dysfunctions including increased locomotor activity, stereotypies, diminished or enhanced response times, and parkinsonian-like features. With the exception of psychomotor impairment and hyperkinesia, MA-induced movement disorders are not well documented in humans. This review attempts to draw parallels between the animal and human changes in basal ganglia neurochemistry associated with MA exposure and offers explanations for why a parkinsonian phenotype is not apparent among individuals who use and abuse MA. Significant differences in the expression of neurotoxicity and presence of multiple environmental and pharmacologic confounds may account for the lack of a parkinsonian phenotype in humans despite evidence of altered dopamine function.

show abstract

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

Cited by 34 publications

References 48 publications

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

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

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

Do Preclinical Findings of Methamphetamine-Induced Motor Abnormalities Translate to an Observable Clinical Phenotype?

Contact Info

Product

Resources

About