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Adolescent-Typical Behavior Patterns 15systems in brain (e.g., intrinsic circuitry interconnecting neurons within a givenbrain region) never becoming myelinated. Moreover, neurons are exquisitely sensitiveto the timing of input (with, for example, glutaminergic activation of NMDAreceptors requiring co-occurring depolarization-dependent changes induced byother ligand/receptor interactions; e.g., see Nestler et al., 2001, for review). Consequently,if converging input pathways vary in whether they become myelinatedor in when that occurs developmentally, the relative speed at which each providesinput to a given common target would vary accordingly during development,potentially influencing the nature of the information being conveyed. Hence, onecould imagine that substantial orchestration of myelination activities might berequired within the context of other ontogenetic changes to permit selective maturationalincreases in speed of information flow while still preserving appropriatetiming of converging inputs.Although less prominent than developmental increases in white matter, ontogeneticdeclines in the relative size of cellular (gray matter) components duringadolescence have been reported in some regions, particularly frontal regions suchas dorsal frontal and parietal areas (Giedd et al., 1999; Rapoport et al., 1999). Thisdecline in gray matter relative to overall volume of particular brain regions is likelyattributable not only to the synaptic pruning seen in these regions during adolescencebut also to ontogenetic increases in white matter (Sowell et al., 1999), withoverall cerebral volume remaining approximately the same from about the age of5 years onward (see Giedd et al., 1996). A decline in gray matter volume is notubiquitous during adolescence, with developmental increases in gray matter volumeseen in certain subcortical regions of the adolescent including the amygdalaand hippocampus (Giedd et al., 1997), as well as in the posterior temporal cortex(see Sowell, this volume).Adolescent-Associated Transformations in Forebrain:Mesocorticolimbic Circuitry, Dopamine, and StressAdolescent Ontogeny of PFCAs reviewed above and detailed in other chapters in this volume, studies usingstructural and functional MRI have revealed evidence for continued developmentand organization of this brain region during adolescence, along with developmentalimprovements in cognitive capabilities (Casey et al., 2000; Lunaet al., 2001; Pine et al., 2002), and affect regulation (see Dahl, 2001, for review).The scope of PFC microstructure and function that can be dissected using imagingtechniques in humans is still limited, however, although technology isimproving rapidly. Thus, to the extent that certain adolescent neural changesand their functional consequences can be modeled in part in other species, studiesin laboratory animals may provide clues as to specific alterations in circuitry