It does remain plausible, however, that the amygdala neurons

we describe here in turn trigger attentional shifts at later stages in processing. It is noteworthy that our ASD subjects were able to perform the task as well as our control subjects, showing no gross impairment. This Vemurafenib was true both when comparing the ASD and non-ASD neurosurgical subjects (see Results), as well as when comparing nonsurgical ASD with their matched neurotypical controls (see Experimental Procedures). RTs for the neurosurgical subjects for experiments conducted in the hospital were increased by approximately 300 ms (Table S9, bottom row) relative to RTs from the laboratory outside the hospital, which is not surprising given that these experiments take place while subjects are recovering from surgery. However, this slowing affected ASD and non-ASD neurosurgical subjects equally.

Alpelisib Unimpaired behavioral performance in emotional categorization tasks such as ours in high-functioning ASD subjects is a common finding that several previous studies demonstrated (Spezio et al., 2007a, Neumann et al., 2006, Harms et al., 2010 and Ogai et al., 2003). In contrast to their normal performance, however, our ASD subjects used a distinctly abnormal strategy to solve the task, confirming earlier reports. Thus, while they performed equally well, they used different features of the face to process the task. Brain abnormalities in ASD have been found across many structures and white matter regions, arguing for a large-scale impact on distributed neural networks and their connectivity (Amaral et al., 2008, Anderson et al., 2010, Courchesne, 1997, Geschwind and Levitt, 2007, Kennedy et al., 2006 and Piven et al., 1995). Neuronal responses in ASD have been proposed to be more noisy (less consistent over time; Dinstein et al., 2012), or to have an altered balance of excitation and inhibition (Yizhar et al., 2011)—putative processing defects that could result

in a global abnormality in sensory perception (Markram and Markram, 2010). The specificity of our present findings is therefore noteworthy: the abnormal feature selectivity of amygdala neurons we found in ASD contrasts with otherwise intact basic electrophysiological properties and whole-face responses. Given the case-study Astemizole nature of our ASD sample together with their epilepsy and normal intellect, it is possible that our two ASD patients describe only a subset of high-functioning individuals with ASD, and it remains an important challenge to determine the extent to which the present findings will generalize to other cases. Our findings raise the possibility that particular populations of neurons within the amygdala may be differentially affected in ASD, which could inform links to synaptic and genetic levels of explanation, as well as aid the development of more specific animal models.