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A role for casein kinase 1 epsilon in the locomotor stimulant response to methamphetamine
Journal article   Peer reviewed

A role for casein kinase 1 epsilon in the locomotor stimulant response to methamphetamine

Camron D Bryant, Melissa E Graham, Margaret G Distler, Michaelanne B Munoz, Dongdong Li, Paul Vezina, Greta Sokoloff and Abraham A Palmer
PSYCHOPHARMACOLOGY, Vol.203(4), pp.703-711
05/01/2009
DOI: 10.1007/s00213-008-1417-z
PMCID: PMC2729782
PMID: 19050854
url
https://www.ncbi.nlm.nih.gov/pmc/articles/2729782View
Open Access

Abstract

We previously colocalized a quantitative trait locus (QTL) for sensitivity to the locomotor stimulant effects of methamphetamine (MA) with a QTL for expression of casein kinase 1 epsilon (Csnk1-E >) in the nucleus accumbens (NAc). Subsequently, we identified a single nucleotide polymorphism in CSNK1E (rs135745) that was associated with increased sensitivity to the subjective effects of d-amphetamine in healthy human subjects. Based on these results, we hypothesized that differential expression of Csnk1-E > causes differential sensitivity to MA-induced locomotor activity in mice. In the present study, we used PF-670462 (PF), which is a selective inhibitor of Csnk1-E >, to directly evaluate the role of Csnk1-E > in the locomotor stimulant response to MA in male C57BL/6J mice. We administered vehicle, PF, MA, or MA + PF, either via intraperitoneal injections or bilateral intra-NAc microinjections. We also examined Darpp-32 phosphorylation in mice receiving intraperitoneal injections. Intraperitoneal PF (20-40 mg/kg) attenuated the locomotor stimulant response to MA (2 mg/kg) without affecting baseline activity. The high dose of PF also significantly inhibited MA-induced phosphorylation of Darpp-32, providing a potential mechanism by which Csnk1-E > contributes to MA-induced locomotor activity. Furthermore, microinjection of PF (5 mu g/side) into the NAc completely blocked the locomotor stimulant response to MA (2.5 mu g/side) without affecting baseline activity. These results provide direct evidence that Csnk1-E > is crucial for the locomotor stimulant response to a moderate dose of MA and suggest that genetic polymorphisms affecting Csnk1-E > expression or function could influence sensitivity to amphetamines in both mice and humans.
Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology Pharmacology & Pharmacy Psychiatry Science & Technology

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