, 1978 and Neale and Cardon, 1992). This method can be used further to determine the magnitude of genetic and environmental covariance between phenotypes; in other words, it is possible to estimate the degree to which phenotypes share common genetic and/or environmental influences. These estimates refer to genetic and environmental correlations, respectively. Utilizing cortical surface reconstruction and spherical atlas mapping procedures developed by Dale and colleagues (Dale et al., 1999 and Fischl et al., buy Depsipeptide 1999b), we mapped each

individual’s surface reconstruction into atlas space. Maps of subject-specific areal expansion or contraction were then computed based on the local stretching or compression needed to map the subject’s surface into atlas space (Rimol et al., 2010a). Next, to examine

patterns of relative surface expansion, we divided the area measure at each location by the total surface area for each participant. The normalized data more directly correspond to the approach used in the animal literature (Bishop et al., 2000 and Paxinos and Watson, 2007) and make it possible to examine genetic influences on cortical regionalization after accounting for global effects. Although registration selleck chemical with atlas space is driven by cortical folding patterns, there is evidence that the folds are good predictors of the locations of functionally distinct regions (Fischl et al., 1999b). Genetic correlations among measures of relative areal expansion at different points on the cortical surface reflect shared genetic influences on surface area between cortical regions and for this reason were used to depict the genetic patterning of the cortex in this study. We used three complementary

approaches to explore the genetic patterns: (1) a hypothesis-driven, seed-based approach; (2) a “marching seed” approach; and (3) a hypothesis-free clustering approach. For the hypothesis-driven, seed-based approach, four seed points were placed at locations presumed homologous to the mouse “functional domains.” The V1 and S1 seed points were placed in the calcarine sulcus and postcentral gyrus, respectively. In order to adjust for the considerable expansion of human frontal and temporal cortices relative to those in the mouse, we also placed seed points in the rostral end of the frontal cortex (frontal pole) and temporal cortex (temporal pole). heptaminol We then created maps of genetic correlations between each of these seed regions and all other locations in the cortex. To address potential bias due to the selection of seed regions, and to assess the sensitivity of the patterns to the exact locations of the seed points, we next used a grid of regularly spaced marching seeds distributed across the entire lateral aspect of one cortical hemisphere. Furthermore, we performed additional fine-grained one-dimensional marching seed analyses to identify gradual or abrupt transitions of the genetic patterning (Cohen et al., 2008).