Molecular and cellular mechanisms of dopamine-mediated behavioral plasticity in the striatum.

The striatum is the input structure of the basal ganglia system. By integrating glutamatergic signals from cortical and subcortical regions and dopaminergic signals from mesolimbic nuclei the striatum functions as an important neural substrate for procedural and motor learning as well as for reward-guided behaviors. In addition, striatal activity is significantly altered in pathological conditions in which either a loss of dopamine innervation (Parkinson's disease) or aberrant dopamine-mediated signaling (drug addiction and L-DOPA induced dyskinesia) occurs. Here we discuss cellular mechanisms of striatal synaptic plasticity and aspects of cell signaling underlying striatum-dependent behavior, with a major focus on the neuromodulatory action of the endocannabinoid system and on the role of the Ras-ERK cascade.