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).
Homeostatic plasticity in living embryonic networks
Understanding the compensatory plasticity that is triggered following perturbations to SNA (e.g. following fetal exposure to GABAergic modulators) will be important in understanding and avoiding disorders of the developing nervous system.