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Timely release of dopamine (DA) at the striatum seems to be important for reinforcement learning (RL) mediated by the basal ganglia. Houk et al. (in: Houk et al (eds) Models of information processing in the basal ganglia, (1995) proposed a cellular signaling pathway model to characterize the interaction between DA and glutamate pathways that have a role in RL. The model simulation results, using GENESIS KINETIKIT simulator, point out that there is not only prolongation of duration as proposed by Houk et al. (1995), but also an enhancement in the amplitude of autophosphorylation of CaMKII. Further, the autophosphorylated form of CaMKII may form a basis for the "eligibility trace" condition required in RL. This simulation study is the first of its kind to support the comprehensive theoretical proposal of Houk et al. (1995).

The activity of mid brain dopamine (DA) neurons resembles the reward prediction error signal of the Temporal Difference (TD) model. Dopamine acting at Dl receptor activates adenylate cyclase through the coupling of Dl receptors with G s / o l f • The complex of adenylate cyclase activates and increases the intracellular levels of cAMP and thereby stim ulating cAMP dependent protein kinase and increasing the state of phosphorylation of DARPP-32 (dopamine and cyclic AMPregulated phosphoprotein, M, = 32,000). DARPP-32 plays an important role in autophosphorylation of calcium calmodulin dependent protein kinaseII (CaMKII) which is crucial for prolongation of long term potentiation (LTP). Here we verified the effect of pre-synaptic re-uptake of dopamine by dopamine transporter on the phosphorylation of DARPP-32 and found that the phosphorylation of DARPP-32 is unaffected by presynaptic re-uptake. Further we have seen that the DARPP-32 phosphorylation does not change with the change in the DA or DIR concentrations.