ABSTRACT
The function of cytoskeletal proteins in slow-transport is to maintain the axon per se, ensuring the structure involved in fast-transport and possibly also generating the driving force of the transport. Extensive introduction of radioisotopes and electron microscopy in the 1960s greatly facilitated the subsequent study of axoplasmic transport. Axonal cytoskeleton as seen by slow transport exhibits compositional variation to a considerable extent. Changes in the rate of axoplasmic transport during development have been examined by several workers. Radioautographic analyses indicate that the great majority of slowly moving materials is retained in the axons, whereas fast-transport is mainly confined to the synaptic terminal. Fast-transport is assigned to the renewal of various membraneous components such as synaptic vesicles, presynaptic and axolemmal plasma membranes, mitochondria, and endoplasmic reticulum. The function of cytoskeletal proteins in slow-transport is to maintain the axon per se, ensuring the structure involved in fast-transport and possibly also generating the driving force of the transport.
