Physiology and Pathophysiology of Axonal Transport

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About 10 members of kinesin family were characterized molecularly, and it was confirmed that axonal cytoskeleton was not transported in the polymerized form (Hirokawa). Fast axonal transport was inhibited by acetylcholine and augumented by adrenaline in the sympathetic neurons in culture (Takenaka). The activity of acetylcholinesterase was found to be different in the neurons sending their axons to mouth-opening muscle from those to closing one in the rat (Amano). Axonal dystrophy in the old monkey gracile nuclei was different morphologically from those in the rat (Fuzisawa). Axonal structure was analyzed in the Aplysial neurons in relation to axonal transport (Koike). In cultured neurons, fast axonal transport was inhibited by light irradiation to the elongating tip of neurite (Goto), and axonal microtubule were stabilized in relation to axonal maturation (Komiya). Fast axonal transport was suggested to be impaired in several motor neuron diseases (Toyoshima), microtubular stability was decreased in biopsy specimens of human sural nerve with several neurological disorders (Oka), and a few morphologacal changes were shown in the transplanted nerves, suggesting the changes of fast axonal transport (Kohshima). Phosphorylation of neurofilament proteins was found decreased in the initial phase soon after administration of IDPN (Komiya), retrograde axonal tranaport was suggested to be decreased in the beta-bromophenylacetylurea treated rat (Oka), and fast axonal transport was impaired in the experimental diabetic rat especially when exposed to hypoxic stress (Nagata).