of grey matter density (Gotgay & Thompson, this issue). Moreover, as Paus (this issue) points out, the extent to which increases in white matter are due to changes in myelin versus changes in axonal diameter is not yet known; although both would improve the flow of information across neural pathways, changes in axonal caliber may have implications for particular neurotransmission processes. However, regardless of whether the absolute extent of synaptic pruning to take place in the prefrontal cortex during adolescence is somewhat smaller than had been believed, the basic notion that the density of prefrontal grey matter follows a ⋂-shaped trajectory over development, with a peak somewhere around age 11 (earlier for girls, later for boys) still finds considerable empirical support and therefore continues to direct our attention to the study of behavioral phenomena in adolescence that are linked in one way or another to prefrontal functioning. That said, there is also growing evidence that important changes occur during adolescence in other brain regions, including the parietal and temporal cortices, as well as the cerebellum. The implications of these structural changes for adolescent behavioral development are far less understood than are those involving the prefrontal cortex.
