Figure 1.

Mouse imaging can bridge the gap between microscale models of brain function and clinical research of macroscale functional connectivity. Mouse models provide a powerful reductive platform that can be employed to link etiological determinants of ASD, such as syndromic mutation or neurodevelopmental traits, to basic molecular and cellular signatures of pathology (left, top to down). However, until recently we have been unable to use this approach to study the neurobiological underpinnings of macroscale functional connectivity, owing to difficulty in translating models of brain function across levels of inquiry. This results in a major explanatory gap between clinical research (heavily relying on macroscale neuroimaging measures of brain function, such as rsfMRI) and preclinical neurobiological investigation in rodent models (bottom, right). The implementation of functional connectivity mapping via rsfMRI in the mouse (right) can bridge this gap, by permitting to causally relate connectional changes with basic molecular or cellular processes, and by permitting a direct translation of these findings from and to humans owing to the shared biophysical principle underlying these measurements (figure adapted from Arguello and Gogos, 2012; Anticevic et al., 2013 with permission).