J. Neurochem. (2011) 10.1111/j.1471‐4159.2011.07281.x Abstract As a ubiquitous serine/threonine protein kinase, glycogen synthase kinase 3β (GSK‐3β) has been considered to be important in the synaptic plasticity that underlies dopamine‐related behaviors and diseases. We recently found that GSK‐3β activity in the nucleus accumbens (NAc) core is critically involved in cocaine‐induced behavioral sensitization. The present study further explored the association between the changes in GSK‐3β activity in the NAc and the chronic administration of methamphetamine. We also examined whether blocking GSK‐3β activity in the NAc could alter the initiation and expression of methamphetamine (1 mg/kg, i.p.)‐induced locomotor sensitization in rats using systemic administration of lithium chloride (LiCl, 100 mg/kg, i.p) and brain region‐specific administration of the GSK‐3β inhibitor SB216763 (1 ng/side). We found that GSK‐3β activity increased in the NAc core, but not NAc shell, after chronic methamphetamine administration. The initiation and expression of methamphetamine‐induced locomotor sensitization was attenuated by systemic administration of LiCl and direct infusion of SB216763 into the NAc core, but not NAc shell. These results indicate that GSK‐3β activity in the NAc core mediates the initiation and expression of methamphetamine‐induced locomotor sensitization, suggesting that GSK‐3β may be a potential target for the treatment of psychostimulant addiction.

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