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Neuromechanics of neuronal transport

Taher Saif (University of Illinois at Urba), Wylie Ahmed (University of Illinois at Urbana-Champaign), Alireza Tofangchi (University of Illinois at Urbana-Champaign)

Mechanics and Physics of Biological Cells

Mon 9:00 - 10:30

Barus-Holley 166

A large majority of neurons have a long axon that forms junctions (synapse) with muscle tissue or another neuron. They carry neurotransmitters enclosed within vesicles that are about 50nm in size. Clustering of vesicles at the synapse is essential for neurotransmission and hence memory and learning. We showed earlier, using embryonic Drosophila (fruit fly), that axons actively maintain a rest tension of about 1 nN. Without this tension, clustering disappears, but reappears with the application of tension. Increase of tension results in increased clustering. Here we explore the role of tension or stretch on vesicle transport along the axon. We use of Aplysia as a model system in this study. We analyze the dynamics of an ensemble of vesicles using the framework of statistical mechanics. We find that the vesicles move along the axon in two modes: (1) random walk (passive motion), and (2) directed motion (active), transported by molecular motors. With increased tension or stretch, vesicles spend more time in active mode compared to that of random walk. Furthermore, increased stretch results in an increased flux of vesicles along the axon. It thus appears that the axonal transport is modulated by the net tension in the axons. In search of the origin of tension in axons, we employed a series of drugs. We find, tension is most likely generated by myosin II motors acting on cortical actin. This corticle actin-myosin complex is distributed along the entire length of the axon, and participates in tension generation. Microtubules play a relatively minor role. Thus, disruption of myosin II, or the filamentous actin, or depletion of ATP results in a loss of tension in axon. Disruption of microtubules shows little effect. It thus appears that the corticle actin, together with myosin II, provide a taut peripheral structure for aligned microtubule tracks for vesicle transport along the axon, and hence clustering at the synapse.