James L. Salzer

Our laboratory investigates the interactions between axons and glial cells that drive assembly of myelinated fibers.  Disruption of these interactions contributes to neurological disorders including multiple sclerosis.  Our goal is to elucidate the biology of these interactions in order to ameliorate demyelination and promote repair in myelin disorders. 

Current studies are focused on several broadly related questions.  First, how do axons drive glial cell differentiation and myelination?  We are characterizing how threshold levels of neuregulin on the axon trigger Schwann cell myelination and determine the number of myelin wraps these glial cells make around axons.

Second, how do myelinating glial cells reciprocally drive the reorganization of axons into electrogenic domains that are essential for proper conduction of action potentials? We are examining the assembly of the axon initial segment (AIS) and nodes of Ranvier, sites of action potential initiation and regeneration, respectively. We are characterizing the cell biology of how these domains form and are investigating activity-dependent plasticity of the AIS, which mediates homeostatic plasticity.

Finally, we are using genetic fate mapping strategies to examine the contributions of adult neural stems to the repair/remyelination of demyelinated axons in the adult CNS. We are particularly interested in the role of the Sonic hedgehog pathway in regulating stem cell repair and interactions of stem cells with microglia during demyelination/remyelination.