Abstract
Autism is a neurodevelopmental disorder clinically characterized by deficits in communication, lack of social interaction and repetitive behaviors with restricted interests. A number of studies have reported that sensory perception abnormalities are common in autistic individuals and might contribute to the complex behavioral symptoms of the disorder. In this context, hearing incongruence is particularly prevalent. Considering that some of this abnormal processing might stem from the unbalance of inhibitory and excitatory drives in brain circuitries, we used an animal model of autism induced by valproic acid (VPA) during pregnancy in order to investigate the tonotopic organization of the primary auditory cortex (AI) and its local inhibitory circuitry. Our results show that VPA rats have distorted primary auditory maps with over-representation of high frequencies, broadly tuned receptive fields and higher sound intensity thresholds as compared to controls. However, we did not detect differences in the number of parvalbumin-positive interneurons in AI of VPA and control rats. Altogether our findings show that neurophysiological impairments of hearing perception in this autism model occur independently of alterations in the number of parvalbumin-expressing interneurons. These data support the notion that fine circuit alterations, rather than gross cellular modification, could lead to neurophysiological changes in the autistic brain.
Highlights
Autism is a neurodevelopmental disorder that affects approximately 1 in 88 children and produces a wide range of sensory, motor and integrative behavioral deficits (Leekman et al, 2007)
Because the area of each electrode array extended beyond auditory cortex (AI), encompassing AI and surrounding auditory cortical regions, we reconstructed AI maps using a subset of 287 responsive sites in the control group and 256 sites in the valproic acid (VPA) group (Figure 2A)
Our results showed that AI maps obtained from VPA rats had significantly higher tonotopic index than controls, indicating a more disorganized map in rats prenatally exposed to VPA (Figure 2C; VPA = 0.28 ± 0.03, Controls = 0.11 ± 0.01; Student’s t-test, p = 0.0004)
Summary
Autism is a neurodevelopmental disorder that affects approximately 1 in 88 children and produces a wide range of sensory, motor and integrative behavioral deficits (Leekman et al, 2007). Autistic children can show severe intellectual disability with seizures to intense social aversion and frequent stereotypies or, in some cases, a less incapacitating profile of mild social retraction with typical-to-high intellectual performance (Lai et al, 2014). Such heterogeneity of profiles is partly due to the existence of multiple etiological factors underlying the autism spectrum disorder (ASD) associated to the current imprecise diagnostic methods that rely basically on behavioral evaluations (Kapur et al, 2012). Genetic and pharmacological models of autism represent an important tool for the characterization of endophenotypes associated with autism and for testing strategies of behavioral rescue
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