Methods to Quantify and Relate Axonal Transport Defects to Changes in C. elegans Behavior

Neuronal growth, differentiation, homeostasis, viability, and injury response heavily rely on functional axonal transport (AT). Erroneous and disturbed AT may lead to accumulation of "disease proteins" such as tau, α-synuclein, or amyloid precursor protein causing various neurological disorders. Changes in AT often lead to observable behavioral consequences in C. elegans such as impeded movements, defects in touch response, chemosensation, and even egg laying. Long C. elegans neurons with clear distinguishable axons and dendrites provide an excellent platform to analyze AT. The possibility to relate changes in AT to neuronal defects that in turn lead to quantifiable changes in worm behavior allows for the advancement of neuropathological disease models. Even more, subsequent suppressor screens may aid in identifying genes responsible for observed behavioral changes providing a target for drug development to eventually delay or cure neurological diseases. Thus, in this chapter, we summarize critical methods to identify and quantify defects in axonal transport as well as exemplified behavioral assays that may relate to these defects.