Expertise
Presynaptic aspects of vertebrate neuromuscular transmission
Mitochondrial Ca2+ handling in motor nerve terminals
Mitochondrial dysfunction in motor nerve terminals of mouse models of familial amyotrophic lateral sclerosis (fALS)
Peripherally-active therapies to preserve neuromuscular function in fALS mice
Discoveries from her lab include (1) contributions of the internodal (submyelin) axolemma and K+ channels to axonal passive and active properties, (2) demonstration that mitochondria in motor nerve terminals temporarily sequester Ca2+ during repetitive nerve stimulation, and that their later extrusion of this Ca2+ produces post-tetanic potentiation, and (3) demonstration of early mitochondrial dysfunction in motor nerve terminals of mice expressing mutant human superoxide dismutase I, a model of amyotrophic lateral sclerosis.
Our laboratory studies ways to preserve neuromuscular structure and function in the SOD1G93A mouse model of amyotrophic lateral sclerosis. We infuse candidate protective agents into one hind-limb and compare neuromuscular structure and function in infused vs. non-infused limbs.