Andreas Frick is Research Director at INSERM (French NIH) and heads the Cortical Plasticity group at the Neurocentre Magendie in Bordeaux. His research focuses on identifying neocortical cellular and circuit mechanisms subserving cognitive abilities or sensory symptoms in autism. His work has been highlighted in national newspapers (e.g., Le Figaro) and specialist magazines. In 2019, Andreas obtained the Marcel Dassault Prize – the highest prize in France for innovative research in mental health disorders. He obtained his Ph.D. in neuroscience from the Max-Planck-Institute for Psychiatry and the Technical University of Munich, and received an Alexander von Humboldt fellowship for his postdoctoral research with Daniel Johnston (Baylor College of Medicine). He held a research group leader position at the Max Planck Institute for Medical Research (Heidelberg), headed by Nobel Laureate Bert Sakmann, prior to moving to Bordeaux.

Talk Title:

Altered sensory perception in the framework of neocortical noise in autism

Abstract:

Altered sensory processing is almost universally experienced by autistic individuals and strongly correlates with the development of other core autism symptoms. One of the hallmarks of this altered sensory processing is an excessive neural and behavioral variability. But what is the neural substrate of this variability? While exploring the underlying basis of atypical tactile processing in the somatosensory cortex in a mouse model of autism, we realized that it was characterized by features of neuronal endogenous noise that could explain many aspects of variable sensory perception (Bhaskaran et al., Nature Communications, accepted). To explore this further, we developed a novel, translational, perceptual decision-making task based on the presentation of vibrotactile stimuli combined with measurements of neocortical population activity in Fmr1-/y mice. These mice displayed perceptual hyposensitivity and increased perceptual variability to vibrotactile stimuli of varying intensities, findings that recapitulate those reported in autistic individuals. Interestingly, this hyposensitivity seemingly contrasts with neuronal hyperexcitability of excitatory neocortical neurons, which together with inhibitory neurons revealed atypical patterns of activity underlying perceptual alterations. These findings provide a preclinical framework for understanding the sources of endogenous noise and its contribution to core autism symptoms, and for relating sensory-related neuronal activity to sensory perception.