The development of static and dynamic perception for stimuli requiring different levels of neural analysis was assessed by measuring orientation-identification and direction-identification thresholds for both lower-level [or first-order (FO)] and higher-level [or second-order (SO)] stimuli as a function of age. Results demonstrate that both lower-level and higher-level perception continue to develop during school-age years in both dynamic and static domains. When compared with adult levels, dynamic performance for 5-6-year-olds is significantly decreased for SO, but not for the FO perception; however, type of stimulus (FO vs. SO) did not affect the development of static perception. We therefore suggest that levels of stimulus complexity should be considered an important variable when assessing and making inferences regarding the typical and atypical development of static and dynamic perception.

We have previously described (see companion paper, this issue) the utility of using perceptual signatures for defining and dissociating condition-specific neural functioning underlying early visual processes in autism and FXS. These perceptually-driven hypotheses are based on differential performance evidenced only at the earliest stages of visual information processing, mediated by local neural network functioning. In this paper, we first review how most large-scale neural models are unable to address atypical low-level perceptual functioning in autism, and then suggest how condition-specific, local neural endophenotypes (described in our companion paper) can be incorporated into causal models to infer target candidate gene or gene clusters that are implicated in autism's pathogenesis. The usefulness of such a translational research approach is discussed.

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The functional link between genetic alteration and behavioral end-state is rarely straightforward and never linear. Cases where neurodevelopmental conditions defined by a distinct genetic etiology share behavioral phenotypes are exemplary, as is the case for autism and Fragile X Syndrome (FXS). In this paper and its companion paper, we propose a method for assessing the functional link between genotype and neural alteration across these target conditions by comparing their perceptual signatures. In the present paper, we discuss how such signatures can be used to (1) define and differentiate various aspects of neural functioning in autism and FXS, and subsequently, (2) to infer candidate causal (genetic) mechanisms based on such signatures (see companion paper, this issue).

Our current understanding of how the visual brain develops is based largely on the study of luminance-defined information processing. This approach, however, is somewhat limiting, since everyday scenes are composed of complex images, consisting of information characterized by physical attributes relating to both luminance and texture. Few studies have explored how contrast sensitivity to texture-defined information develops, particularly throughout the school-aged years. The current study investigated how contrast sensitivity to luminance- (luminance-modulated noise) and texture-defined (contrast-modulated noise) static gratings develops in school-aged children. Contrast sensitivity functions identified distinct profiles for luminance- and texture-defined gratings across spatial frequencies (SFs) and age. Sensitivity to luminance-defined gratings reached maturity in childhood by the ages of 9–10 years for all SFs (0.5, 1, 2, 4 and 8 cycles/degree or cpd). Sensitivity to texture-defined gratings reached maturity at 5–6 years for low SFs and 7–8 years for high SFs (i.e., 4 cpd). These results establish that the processing of luminance- and texture-defined information develop differently as a function of SF and age.