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16 BIOLOGICAL AND SOCIAL UNIVERSALSwithin the PFC and associated networks during adolescence. When using suchanimal models, however, it is important to consider potential species differencesin the homology of particular brain regions and the comparability of their organization(Preuss, 2000).Several adolescent-associated alterations in PFC characterized in human adolescentshave been observed in adolescents of other mammalian species as well.For instance, volumetric declines in PFC gray matter have been reported notonly in humans (e.g., Sowell et al., 1999) but also in rats (van Eden et al., 1990).Likewise, synaptic pruning of presumed glutaminergic excitatory input is observedduring adolescence in humans (Huttenlocker, 1984) and nonhuman primates(Zecevic et al., 1989), with decreases in number of glutamate receptorsof the NMDA receptor subtype observed in the cortex of rats during adolescenceas well (Insel et al., 1990). Complementary to the decline in excitatoryglutaminergic drive to cortex (Zecevic et al., 1989), dopaminergic (DA) inputto certain portions of the PFC increases during adolescence in nonhuman primatesto peak at levels considerably higher than those seen earlier or later inlife (e.g., Rosenberg & Lewis, 1995). Studies in rats also have revealed developmentalincreases through adolescence in a number of measures of DA inputto PFC, including DA fiber density (Benes et al., 2000) and DA concentrations(Leslie et al., 1991). Recent rodent studies have also linked adolescence withimportant changes in DA modulation within PFC. For instance, there is a lossof “buffering capacity” among DA terminals in PFC during adolescence that isassociated with the disappearance of DA autoreceptors, which in the juvenilehad formed part of a negative feedback system to regulate rates of DA synthesis(Dumont et al., 2004). Also, PFC slices from adolescent rats do not showadult-typical depolarization in response to coactivation of DA D1 receptors andNMDA receptors, even though this depolarized “up state” is thought to be criticalfor information processing and plasticity (Tseng & O’Donnell, 2005). Functionalimplications of these ontogenetic alterations in DA activity and modulatorycapacities in the PFC have yet to be characterized and may need to be interpretedwithin a broader context of adolescent-associated alterations in DA activityin other brain regions, as discussed next.The Adolescent DA System and Developmental Shiftsin the Balance Between Mesocorticaland Mesolimbic/Striatal DA SystemsAlterations in DA activity in forebrain regions during adolescence are not restrictedto the mesocortical DA system projecting to PFC but are also evident in DA projectionsto the striatum as well as the mesolimbic DA system (i.e., DA projectionsto limbic areas such as the nucleus accumbens and amygdala). One notable andwell-substantiated change is the decline in DA receptors seen during adolescence