Abstract

Changes in the timing performance of conditioned responses (CRs) acquired during trace and delay eyeblink conditioning (EBC) are presented for diagnostic subgroups of children having autism spectrum disorder (ASD) aged 6–15 years. Children diagnosed with autistic disorder (AD) were analyzed separately from children diagnosed with either Asperger’s syndrome or Pervasive developmental disorder (Asp/PDD) not otherwise specified and compared to an age- and IQ-matched group of children who were typically developing (TD). Within-subject and between-groups contrasts in CR performance on sequential exposure to trace and delay EBC were analyzed to determine whether any differences would expose underlying functional heterogeneities of the cerebral and cerebellar systems, in ASD subgroups. The EBC parameters measured were percentage CRs, CR onset latency, and CR peak latency. Neither AD nor Asp/PDD groups were impaired in CR acquisition during trace or delay EBC. Both AD and Asp/PDD altered CR timing, but not always in the same way. Although the AD group showed normal CR timing during trace EBC, the Asp/PDD group showed a significant 27 and 28 ms increase in CR onset and peak latency, respectively, during trace EBC. In contrast, the direction of the timing change was opposite during delay EBC, during which the Asp/PDD group showed a significant 29 ms decrease in CR onset latency and the AD group showed a larger 77 ms decrease in CR onset latency. Only the AD group showed a decrease in CR peak latency during delay EBC, demonstrating another difference between AD and Asp/PDD. The difference in CR onset latency during delay EBC for both AD and Asp/PDD was due to an abnormal prevalence of early onset CRs that were intermixed with CRs having normal timing, as observed both in CR onset histograms and mean CR waveforms. In conclusion, significant heterogeneity in EBC performance was apparent between diagnostic groups, and this may indicate that EBC performance can report the heterogeneity in the neurobiological predispositions for ASD. The findings will inform further explorations with larger cohorts, different sensory modalities, and different EBC paradigms and provide a reference set for future EBC studies of children having ASD and non-human models.

Highlights

  • The purpose of this paper is to describe the changes in conditioned response (CR) performance during trace and delay eyeblink conditioning (EBC) in a cohort of high-functioning children having autism spectrum disorder (ASD)

  • Switching to delay EBC did not significantly change the percentage CRs from the previous session (Figure 1B), and there was no significant difference between groups as the overall mean CR frequency during delay EBC was 48 ± 4, 41 ± 7, and 46 ± 8% for typically developing (TD), autistic disorder (AD), and Asperger’s syndrome or Pervasive developmental disorder (Asp/PDD), respectively [F(2,27) = 0.1, p = 0.93 for the first three blocks; F(8,216) = 0.5, p = 0.63 for all nine blocks]

  • There was no indication that AD or Asp/PDD impaired the ability to acquire CRs during trace or delay EBC or show asymptotic percentage CRs characteristic of the TD group under these EBC

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Summary

Introduction

The purpose of this paper is to describe the changes in conditioned response (CR) performance during trace and delay eyeblink conditioning (EBC) in a cohort of high-functioning children having autism spectrum disorder (ASD). We provide more detailed information regarding the distribution of CR performance changes in the cohort described by Oristaglio et al (1), re-grouped by ASD-spectrum diagnosis in order to determine whether heterogeneity in EBC performance may relate to diagnostic category within a high-functioning group of children. Two previous studies (1, 3) of subjects having idiopathic ASD demonstrated changes in CR timing during delay EBC without a reduction in the rate of CR acquisition, agreeing that CR timing is shifted earlier with ASD. Four studies have demonstrated heterogeneity in the changes in EBC performance among individuals with varying ASD symptomatology. This heterogeneity is mirrored in mouse models of idiopathic and syndromic ASD in which there are differential changes in the rate of CR acquisition and the directionality of CR timing that depend on the specific gene mutation induced (4, 6, 7)

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