Sumantra Chattarji
Centre for High Impact Neuroscience and Translational Application, Kolkata
Sumantra Chattarji is the Founding Director of a new translational neuroscience institute called CHINTA at TCG CREST. He is a Visiting Professor at Simons Initiative for the Developing Brain, University of Edinburgh, UK. He received his PhD in Neuroscience at the Johns Hopkins University and Salk Institute. After post-doctoral research at Yale University and MIT, he started his own laboratory at the National Centre for Biological Sciences, TIFR, Bangalore, India in 1999. His research has shown how changes in brain cells give rise to emotional symptoms of stress-related psychiatric disorders. His lab also studies the neural basis of autism, research for which he was awarded the Global Champion Award by the Fragile X Research Foundation, USA. He is a Fellow of the Indian Academy of Sciences, International Union of Physiological Sciences and European Molecular Biology Organization. He also served on the Council of the Society for Neuroscience, the first Indian to do so.
Session 2C: Symposium – “Brain Function in Health and Disease”
Sumantra Chattarji - CHINTA, Kolkata
“Astro”logy in Autism
Important insights into the pathophysiology of fragile X syndrome (FXS), a common monogenic cause of autism spectrum disorder, have emerged from analyses of rodent models. These findings, however, have been less effective in developing therapeutic interventions, thereby highlighting the need for model systems of human origin. Moreover, many studies have focused on neurons, and the role of glia remains largely unexplored in FXS. We used human pluripotent stem cells to examine the potential role of astrocytes in physiological abnormalities in FXS neurons. FXS cortical neurons, co-cultured with FXS astrocytes, fired spontaneous bursts of action potentials that are more frequent, but shorter in duration, compared to control neurons co-cultured with control astrocytes. However, bursts fired by FXS neurons, co-cultured with control astrocytes, are indistinguishable from control neurons. Conversely, control neurons exhibit aberrant firing in the presence of FXS astrocytes. Thus, the genotype of astrocytes determines the physiological phenotype of neurons. Strikingly, astrocytic conditioned medium by itself, from either control or FXS astrocytes is capable of eliciting the same spontaneous burst firing patterns that would be observed if astrocytes were physically present in co-cultures. By analysing the mechanistic basis of this effect, we identify an important cell non-autonomous contribution of astrocytes in correcting aberrant electrical activity in human FXS neurons. Thus, this work suggests a novel framework for exploring therapeutic strategies aimed at neuron-glia interactions.