Salzer Lab

1. How do reciprocal interactions between axons and glia drive assembly of myelinated axons?

We are characterizing both juxtacrine and paracrine signals between axons and glial that regulate myelination; these signals are candidates to drive demyelination under pathological conditions.

2. How do myelinating glial cells 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, how their assembly is coordinated with myelination, and are investigating activity-dependent plasticity of the AIS, which mediates homeostatic plasticity.

3. Elucidating the pathology of demyelination and the contributions of adult neural stem cells (NSCs) to remyelination in the adult CNS.

We are particularly interested in the role of the Sonic hedgehog pathway in regulating stem cell repair in the CNS and PNS and the interactions of NSCs with microglia during demyelination and remyelination.

Methods

For these various studies, we use primary neuron and myelinating cocultures, novel transgenic/knockout mice including those undergoing toxin or autoimmune-medated demyelination, and employ various imaging modalities (EM/immuno-EM, live imaging, STORM, serial block face reconstructions, etc.) to further parse mechanisms that mediate these events.