Objectives: We designed our study to extend previous studies of conditioned learning in ASC in two key ways: first, we included a lengthier extinction period in order to better examine the time it takes to learn and then to extinguish the new learning (which involves amygdala and orbitalfrontal cortex); second, we manipulated the emotional valence of the conditioned stimulus to compare the facilitation of social/emotional meaning on learning, across ASC and comparison groups.
Methods: Four groups of 15 individuals (two ASC and two comparison groups) completed a simple conditioned learning task that used a 1000ms white noise burst as the unconditioned, aversive stimulus. Two groups (one ASC, one comparison) did the task using neutral, colored squares as the conditioned stimuli (CS); the other groups did the same task but with the colored squares replaced by angry faces. Dependent measures were the difference scores in galvanic skin response (GSR) and heart rate (HR) in response to the safe (non-reinforced) CS versus the threatening (followed by the white noise) CS.
Results: The ASC groups did show conditioned learning in GSR and HR measures, but this learning was significantly slower than the comparison group (i.e., the peak difference score occurred later in the task); extinction was also intact but, subsequently to longer initial learning, also took longer to extinction. In the comparison group, the face stimuli facilitated conditioning as evidenced by a) faster conditioning (peak occurred earlier in the task); b) stronger conditioning (larger peak magnitudes of difference between threat and safe conditions); and c) prolonged activation to the threat stimulus, which delayed extinction. The ASC group, however, demonstrated significantly less facilitation by the face stimuli, showing a response more similar to that evoked by the more neutral colored squares.
Conclusions: We extended research regarding basic behavioral mechanisms of amgydala function in ASC by allowing more time for the conditioned response to occur, and by manipulating the influence of stimulus type in conditioned learning experiments. Our findings suggest that amygdala impairment in ASC may reflect more widespread difficulties elsewhere in the brain, or in connectivity to other brain systems, rather than primary dysfunction in the amygdala itself. That is, fundamental amygdala function (necessary for conditioned learning) is intact but is moderated by other factors of learning speed and social perception.