We're looking forward to you joining us (virtually) for the SC Program Meeting, Thursday October 1 at 2:00 on Zoom. This week Gina Turrigiano, Brandeis University (and Stanley Center SAB member) will be speaking, hosted by Jen Pan. All Broadies are welcome! 
 

"Keeping your E/I balance in an uncertain world: firing rate homeostasis and Shank3"  

Gina Turrigiano, Joseph Levitan Professor of Vision Science, Brandeis University 

Gina Turrigiano holds the Joseph Levitan Chair in the Dept. of Biology at Brandeis. She has received numerous awards for her research including a MacArthur foundation "genius" award, McKnight Foundation Technological Innovation and Neurobiology of Disease awards, an NIH director’s pioneer award, and the HFSP Nakasone Award. She is a fellow of the American Academy of Arts and Sciences, a Fellow of the American Association for the Advancement of Science, and a member of the National Academy of Sciences. Her scientific interests include mechanisms of synaptic and intrinsic plasticity and the experience-dependent rewiring of neocortical microcircuitry.

Talk abstract: 

Neocortical networks must generate and maintain stable activity patterns despite perturbations induced by learning and experience- dependent plasticity. There is abundant theoretical and experimental evidence that network stability is achieved through homeostatic plasticity mechanisms that adjust synaptic and neuronal properties to stabilize some measure of average activity, and this process has been extensively studied in primary visual cortex (V1), where chronic visual deprivation induces an initial drop in activity and ensemble average firing rates (FRs), but over time activity is restored to baseline despite continued deprivation. Here I discuss recent work from the lab in which we followed this FR homeostasis in individual V1 neurons in freely behaving animals during a prolonged visual deprivation/eye-reopening paradigm. We find that – when FRs are perturbed by manipulating sensory experience – over time they return precisely to a cell-autonomous set-point. Finally, we find that homeostatic plasticity is perturbed in a mouse model of Autism spectrum disorder, and this results in a breakdown of FRH within V1. These data suggest that loss of homeostatic plasticity is one primary cause of excitation/inhibition (E/I) imbalances in ASD models. Together these studies illuminate the role of stabilizing plasticity mechanisms in the ability of neocortical circuits to recover robust function following challenges to their excitability.