Benjamin A. Eaton, Ph.D.
Our lab is interested in defining the molecular mechanisms that stabilize and maintain synapse function throughout the lifespan of an organism. These mechanisms include stabilization of both synaptic innervations and synaptic transmission. Furthermore, we predict that these mechanisms contribute to age-dependent declines in nervous system function that are observed normally and during disease. Our primarily analysis is performed on the neuromuscular junction of Drosophila in both larvae and adult (see Figure). This system combines high-resolution synaptic analysis with power molecular and genetic approaches. Current projects include:
1) The effects of age and diet on synaptic function. We are using the newly developed synapse system, the CM9 NMJ, to investigate changes to synapse function with age and how these changes contribute to the overall decline in neuromuscular performance observed with age. We are particularly interested in studies focused on changes in the composition and function of ion channels within the nerve terminal and changes to the active zone.
2) How the selective trafficking of components required for normal synaptic function is achieved. The long-term maintenance of synapse function requires the turnover and replacement of synaptic material with age. We are interested in determining the molecules involved in the selective trafficking of presynaptic components. We are particularly interested in microtubule-based transport mechanisms utilizing the dynactin complex. Mutations in DCTN1 result in age-dependent neurological disorders including lower motor disease and frontotemporal dementia.
Rebekah Mahoney, Joel M Rawson and Benjamin A. Eaton. “An age-dependent change in the synaptic homeostasis set point at the NMJ.” Journal of Neuroscience (in press).
Leo Chang, Holly Davison, Tabita Kreko, Rebekah Mahoney, Tim Cusmano, Yimin Wu, Adrian Rothenfluh, and Benjamin A. Eaton. “Genetic dissection of synaptic pathologies in dynactin mutants identifies Arfaptin, a specifier of dynactin complex function during synapse growth.” Molecular Biology of the Cell, June, 2013, vol. 24 (11), pp. 1749-64.
Nina Boiko, Volodymyr Kucher, Benjamin A. Eaton, and James D. Stockand. “Inhibition of Neuronal Deg/ENaC Channels by the Multiple Sclerosis Drug 4-Aminopyridine.” Journal of Biological Chemistry, March 29, 2013, vol. 288 (13), pp. 9418-27.