Normally-behaving neural networks have an amazing capacity to maintain themselves within working activity ranges through homeostatic adjustments to cellular excitability, glutamatergic and GABAergic synaptic strength (homeostatic plasticity).

We study the triggers and mechanisms that underlie these forms of plasticity in developing circuits in order to understand why homeostatic mechanisms are in some cases (spasticity, seizure) incapable of maintaining normal activity levels, and to identify how triggers of homeostatic plasticity could inappropriately lead to hyperexcitable states associated with neural injury and disease (spinal cord injury, autism).