Eugene Meyer III Professor of Neuroscience, Neurology
- MBBS, Medicine, University of Delhi
- PhD, Neuroscience, University of Virginia
- Internship, Internal Medicine, Eastern Virginia School of Medicine
- Residency, Neurology, Medical College of Virginia, Virginia Commonwealth University
- Fellowship, Epilepsy/EEG, University of Michigan
Biology, Biomedical Engineering, Biophysics, Neuroscience, Physiology, Translational Science
Seizures, neuronal excitability and plasticity
1) Seizures as brain explorers: A few thousand neurons acting together can generate a seizure, but it travels far from its origin, generating convulsive and dystonic movements, triggering and erasing memories, causing sadness and depression, altering hormonal cycles, and even suppressing breathing. We study these circuits using activity reporter mice and manipulate them using chemogenetic and optogenetic methods.
2) We recently learned that the brain can sense lactate via a receptor called HCA1 Receptor. Seizures generate a lot of lactate, so we investigated the role of lactate receptors in seizures. Early findings are that the receptor acts to suppress seizures.
3) Most seizures end because the brain has strong inhibitory mechanisms, but they can become self-sustaining, and prolonged to cause death or brain injury, if inhibition breaks down. These seizures, called status epilepticus, represent an extreme form of activity-induced brain plasticity. We found that seizures modulate GABA and AMPA receptor trafficking. These studies prompted interest in clinical trials. We performed an established status epilepticus treatment trial (ESETT), which defines the treatment of status epilepticus when benzodiazepines have failed.