Novel aspects of striatal plasticity associated with long-term levo-dopa administration.

“Striatal plasticity” is a term describing a variety of morphological and functional changes occurring both at preand post-synaptic level within the basal ganglia. In most cases striatal plasticity occurs when a loss of dopamine (DA) fibers in the striatum, in the course of Parkinsonism takes place. Plastic events include early pre-synaptic and long-term post-synaptic changes. In the context of long-term changes associated with striatal plasticity the role of intrinsic striatal catecholamine cells is emerging. This neuronal population expresses both tyrosine hydroxylase (TH) and DA transporter (DAT). These TH-positive cells are normally resident within the human caudate putamen but they dramatically increase during parkinsonism reaching an amount roughly corresponding to 50% of nigrostriatal neurons counted in control brains. This evidence led to hypothesize fascinating mechanisms bridging these neurons either with compensatory changes or the onset of aberrant behavioral activity. Very recently the occurrence of these neurons was described during DA replacement therapy in parkinsonism, thus suggesting that these cells may represent the anatomical basis for plastic phenomena. Thus, the present article, in the attempt to describe novel mechanisms generating striatal plasticity, details these cells in development and adult life and their potential role in maturation phenomena occurring in parkinsonism.