Pharmacogenetics of cocaine: I. Locomotor activity and self-selection

Bc, Jones; Cl, Reed; Ra, Radcliffe; Vg, Erwin

doi:10.1097/00008571-199308000-00002

Cited by 18 publications

(10 citation statements)

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“…By contrast, morphine strongly and dose-dependently activated C57 mice but inhibited DBA mice. Such opposite phenotypes are in accord with data obtained by other studies (Jones et al 1993;Murphy et al 2001;Zocchi et al 1998) and do not support a predictive relationship between the incentive properties and psychomotor-stimulant effects of cocaine or morphine.…”

Section: Discussionsupporting

confidence: 77%

Susceptibility to conditioned place preference induced by addictive drugs in mice of the C57BL/6 and DBA/2 inbred strains

et al. 2005

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Section: Discussionsupporting

confidence: 77%

Susceptibility to conditioned place preference induced by addictive drugs in mice of the C57BL/6 and DBA/2 inbred strains

et al. 2005

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“…Several studies using inbred strains of mice have reported pharmacokinetic differences that could account for differential COC-induced locomotor activation Reith et al, 1987;Wiener and Reith, 1990;Jones et al, 1993). Others have found increased number and affinity of DATs in the NAc of high, compared to low, novelty responders (Chefer et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Individual Differences in Cocaine- and Amphetamine-Induced Activation of Male Sprague–Dawley Rats: Contribution of the Dopamine Transporter

Briegleb

Gulley

Hoover

et al. 2004

Neuropsychopharmacol

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Previously we found that outbred male Sprague-Dawley rats can be classified as either low or high cocaine responders (LCRs or HCRs, respectively), based on their open-field locomotor response to acute cocaine (COC; 10 mg/kg, i.p.). Here, we extended this analysis to amphetamine (AMPH; 0.5, 1, and 5 mg/kg, i.p.) and found that the individual differences in behavioral activation were not as pronounced as with COC. This was confirmed with observational analysis of behaviors. Differences in drug-induced activation could involve differential dopamine transporter (DAT) function/trafficking. To address this possibility, we measured [ 3 H]DA uptake into dorsal striatal synaptosomes prepared from rats injected 30 min earlier with saline, COC, or AMPH to determine DAT activity, and radioligand binding to determine the total number of DATs. Striatal [ 3 H]DA uptake in COC-treated HCRs was significantly higher than in LCRs. Furthermore, regardless of LCR/HCR classification, uptake in individual COC-treated rats was significantly correlated with their locomotor behavior in the 30 min after drug administration. In contrast, AMPH-treated rats did not differ in uptake, nor were uptake and locomotor activity correlated. DAT number did not differ between LCRs or HCRs, or between AMPH-treated rats. In addition, when individual differences in COC-induced behavior were no longer detected in LCRs and HCRs 1 week after initial classification, uptake was also similar. Together, these results suggest that a difference in expression of functional DATs on the cell surface contributes to the individual differences observed in COC-induced, but not AMPH-induced, behavioral activation of rats.

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“…It is difficult to interpret this finding, given the often contradictory results of other studies. For example, some studies have found no difference between B6J and D2J mice (Jones et al 1993;Phillips et al 1998), while others have reported greater activation in the D2J strain (Womer et al 1994;Rocha et al 1998). Still others have reported a more complex behavioral response to cocaine between these two strains, with no differences observed at lower doses, while D2J mice exhibited greater activation at higher doses Carney 1994, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…While some studies, using inbred strains of mice, have reported evidence for pharmacokinetic differences which could account for differential cocaine-induced locomotor activation Reith et al 1987;Wiener and Reith 1990;Reith and Selmeci 1991;Jones et al 1993), others have shown that differences in behavioral sensitivity to cocaine cannot be explained by differences in cocaine disposition (Ruth et al 1988;Womer et al 1993;Rocha et al 1998). To the best of our knowledge, no studies have examined distribution of cocaine in the blood or brain following acute administration in B10SnJ, BR, or L mice; it is possible that the atypical behavioral response to cocaine we observed in these strains may be due, at least in part, to genetically mediated pharmacokinetic differences.…”

Section: Discussionmentioning

confidence: 99%

Genetic variation in the psychomotor stimulant properties of cocaine in Mus musculus

et al. 2003

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The genetic similarity between C57BL/10SnJ and the other closely related C57BL substrains suggests the possibility that the aberrant behavioral response to cocaine observed in B10SnJ mice may be due to a major gene effect. Similarly, the differences found in the C57BR/cdJ and C57L/J substrains may also be influenced by a major gene. The strains examined in this study will be useful tools for identification of relevant quantitative trait loci.

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Pharmacogenetics of cocaine: I. Locomotor activity and self-selection

Cited by 18 publications

References 0 publications

Susceptibility to conditioned place preference induced by addictive drugs in mice of the C57BL/6 and DBA/2 inbred strains

Susceptibility to conditioned place preference induced by addictive drugs in mice of the C57BL/6 and DBA/2 inbred strains

Individual Differences in Cocaine- and Amphetamine-Induced Activation of Male Sprague–Dawley Rats: Contribution of the Dopamine Transporter

Genetic variation in the psychomotor stimulant properties of cocaine in Mus musculus

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