The differential neurobehavioral effects of forebrain dopamine (DA) depletions in neonatal and adult rats are reviewed. In contrast to the severe and long-lasting parkinsonian sensorimotor deficits seen in rats sustaining large DA depletions as adults, rats comparably depleted as neonates are spared from these gross behavioral deficits. While DA released from residual striatal DA terminals remains necessary for the gradual recovery of sensorimotor function in rats lesioned as adults and the sparing from deficits in rats lesioned as neonates, the specific roles of D1- and D2-like receptors differ between the two age groups. Coactivation of striatal D1 and D2 receptors by residual DA is necessary for the expression of sensorimotor behavior in rats depleted of DA as adults (and in intact rats) whereas activation of either D1 or D2 receptors is sufficient for these behaviors in rats depleted of DA as neonates. We discuss the D1/D2 modulation of several important markers for striatal transmission (acetylcholine release from interneurons, induction of c-fos, and the expression of GAD65 mRNA in striatal efferents) as potential mechanisms underlying this striking age-dependent plasticity following forebrain DA depletions.
|State||Published - 1998|