Kyle P. Lillis

This study shows that acute ClC-2 inhibition depolarizes EGABA, increases neuronal intracellular chloride, and alters GABAergic chloride signaling dynamics.

This study evaluates synthetic kainic acid injection parameters in the IHK model to reliably induce seizures while minimizing mortality.

This study examines seizure patterns in a porcine model of post-traumatic epilepsy, finding that seizures start focally and evolve to generalized convulsions with stereotypical behaviors.

The paper measures extracellular chloride concentrations in the brain and finds they are lower and more variable than previously thought due to displacement by immobile anions, affecting GABAA receptor function.

This study identifies the cellular sources of ictal population signals in seizures using calcium imaging and electrophysiology in mouse models.

This paper develops techniques for high-resolution 2-photon imaging of fluorescent proteins in living swine brains, addressing challenges in motion artifact and large animal imaging.

The paper shows that after acute brain injury, microglial phagocytosis becomes overwhelmed, leading to a buildup of dying neurons and highlighting the need for longitudinal assays to accurately measure cell death.

The paper measures chloride ion concentrations in neurons to show the existence of stable cytoplasmic chloride microdomains that affect GABAergic signaling.