In animals exposed to VPA in utero, several autistic-like behaviors tend to appear including reduced social interaction, reduced sensitivity to pain, increased sensitivity to tactile stimuli, diminished acoustic prepulse inhibition, memory impairment/improvement, prolonged repetitive behaviors, altered anxiety and fear behaviors and hyperactivity ( Schneider and Przewlocki, 2005 Markram et al., 2008 Bambini-Junior et al., 2011 Brandão and Romcy-Pereira, Unpublished Edalatmanesh et al., 2013 Kataoka et al., 2013 Kim and Bao, 2013). The valproic acid (VPA) model of autism translates to the animal the prenatal exposure of embryos to the antiepileptic drug VPA, which is shown to significantly increase the odds of autistic births in humans ( Christianson et al., 1994 Rodier et al., 1997 Williams et al., 2001 Miyazaki et al., 2005 Christensen et al., 2013). In rodents, 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. Recent studies also support the idea that sensory dysfunctions in autism may be related to an inhibitory-excitatory imbalance derived from alterations of critical period time course ( Rubenstein and Merzenich, 2003 Le Blanc and Fagiolini, 2011). It is well described in the literature that hearing abnormalities including hyper/hypo-sensitivity, deficits in acuity and incongruence of auditory perception (i.e., distortions) are frequently observed among autistic individuals ( Rosenhall et al., 1999 Davis et al., 2006 Tharpe et al., 2006 Gomes et al., 2008 Madsen et al., 2014). In this context, the development of better diagnostic methods and treatments for subtype-specific forms of autism can benefit from studies aimed to characterize reliable electrophysiological autistic endophenotypes (i.e., physiological or biochemical processes altered in the disorder). 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). Clinically, 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). These data support the notion that fine circuit alterations, rather than gross cellular modification, could lead to neurophysiological changes in the autistic brain.Īutism 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). 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. However, we did not detect differences in the number of parvalbumin-positive interneurons in AI of VPA and control rats. 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. 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. In this context, hearing incongruence is particularly prevalent. 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. 2Montreal Neurological Institute, McGill University, Montreal, QC, CanadaĪutism is a neurodevelopmental disorder clinically characterized by deficits in communication, lack of social interaction and repetitive behaviors with restricted interests.1Brain Institute, Federal University of Rio Grande do Norte, Natal, Brazil.Renata Figueiredo Anomal 1, Etienne de Villers-Sidani 2, Juliana Alves Brandão 1, Rebecca Diniz 1, Marcos R.
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