Professor Sumantra Shona Chattarji is the Director of the Centre for Brain Development and Repair, inStem, Bangalore and a specialist in the neurobiology of learning and memory at the National Centre for Biological Sciences in Bangalore.
Professor of Neurobiology at the National Centre for Biological Sciences in Bangalore, India, Shona is a key collaborator in the Patrick Wild Centre and his lab studies the effects of stressful experiences on neurons and synapses in the amygdala – the brain’s emotional hub.
THE AMYGDALA’S ROLE IN STRESS AND AUTISM SPECTRUM DISORDER
Although we think of memories as rooted in the past, they have a profound influence on how we respond to events in the future. In this sense, what we learn from past experiences — our memories — not only give shape to our sense of who we are, but also how we interact with the world around us.
Memories come in many different flavours — some experiences are memorable, others forgettable. Emotionally significant experiences tend to be well remembered, and the amygdala has a major role in this process. Yet the rapid and efficient encoding of emotional memories can become maladaptive — severe stress can often turn them into a source of prolonged anxiety.
So what are the cellular mechanisms underlying these powerful emotional symptoms? To answer these questions, we have been carrying out a range of behavioural, morphometric, electrophysiological and biochemical analyses of the neural correlates of stress-induced modulation of amygdala structure and function.
Our findings point to unique features of stress-induced plasticity in the amygdala, which are strikingly different from those seen in the hippocampus, and could have long-term consequences for behavioural symptoms seen in affective disorders. Furthermore, the genes we inherit can also cause behavioural dysfunction. Strikingly, individuals afflicted with certain types of autism spectrum disorder often exhibit impaired cognitive function alongside debilitating emotional symptoms. Therefore, we have extended our studies to include genetically engineered rodents so as to identify cellular and molecular targets that can be used to correct symptoms of fragile X syndrome.