• Taku Kawataki, Kaori Osafune, Mari Suzuki, and Tatsuro Koike.
• Molecular Neurobiology Laboratory, Division of Life Science, Hokkaido University, Graduate School of Life Science, North Ward N10W8, Science Building #5, Room 9512, Sapporo 060-0810, Japan.
• Brain Res. 2008 Sep 16; 1230: 37-49.

AbstractNeurite (axon and dendrite) degeneration requires self-destructive programs independent of cell death programs to segregate neurite degeneration from cell soma demise. We have here addressed the question of whether neuritic degeneration is delayed or occurs normally under conditions in which sympathetic neurons acquire resistance to somal apoptosis upon maturation. For this purpose, we have examined both beading formation and fragmentation, two hall-marks of neurite degeneration, caused by three experimental paradigms including NGF deprivation, treatment with microtubule-disrupting agents, and in vitro Wallerian degeneration. Sympathetic neurons from 1-day-old mice or newborn rats were grown for 5-6 days (young) or 3 weeks (mature). Mature neurons acquired resistance to apoptosis caused by colchicine as well as NGF withdrawal. Neither cytochrome c release nor DNA fragmentation occurred. Both beading formation and subsequent fragmentation were delayed in mature neurons following NGF deprivation, treatment with colchicine, or in vitro Wallerian degeneration. Neuritic ATP levels of young ganglia decreased rapidly, while those of mature ganglia did so slowly during degeneration, although the basal levels of neuritic ATP of both ganglia were similar. Notably, mature neurites were resistant to fragmentation caused by NGF deprivation and capable of growing again after replenishment of NGF. This development of resistance to neurite degeneration in mature neurons may be thought as an important protective mechanism for the maintenance of the adult nervous system.

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