Topic: repetitive behaviors

Autism spectrum disorder (ASD) is a lifelong neurodevelopmental disorder characterized by early-onset impairments in social communication, repetitive behaviors and stereotypies. The present study was designed to investigate the developmental alteration of social behavior in rat model of autism induced by valproic acid (VPA). Experiments were carried out on prenatally VPA-treated and control (saline treated) rats at two different ages: adolescent (postnatal day 30) and young-adult (3 months-old) male rats. Sociability was evaluated in a three-chamber apparatus. The results showed that groups of

Dysregulation in the cortico-striatal circuits has been shown to be related to pathologic repetitive behaviors but the underlying dysfunctional mechanisms at the microcircuit level remain under investigation. A key element that regulate the striatal output iare striatal parvalbumin (PV) interneurons which exert a powerful feedforward inhibition on medium spiny neurons. To investigate the role of PV interneurons in regulating aberrant striatal activity observed in repetitive behaviors, we used the Sapap3 mutant mice, which exhibit excessive self-grooming. Using optogenetics activation of PV int

Autism spectrum disorder (ASD) is a neurodevelopmental disorder associated with social communication deficits, repetitive behaviors, and atypical sensory responses. Around 90% of the patients diagnosed with ASD experience atypical sensory events, with abnormal responses to tactile stimulation. However, the neurological underpinnings of tactile dysfunction in ASD are not yet understood. Using behavior and electrophysiological in vivo recordings, this work aims to promote a better understanding on tactile sensitivity and neuronal responses to glabrous skin tactile stimulation in Shank3 KO mouse

Diverse neurodevelopmental syndromes (e.g. Fragile X) are caused by alterations in specific genes leading to pervasive impairments comorbid with autism (i.e. social and repetitive behaviors). Although all ASDs converge into common core behaviors, genetic variants in ASD are very heterogeneous. Here, we describe a cleavable cell adhesion molecule (Negr1) as upregulated in the brain of 5 diverse mouse models of ASDs (including Fragile X) and postmortem brains from people with autism or Fragile X, and causative of core ASD behaviors and brain alterations when up-regulated in wild-type (WT) animal