Differential effects of depolarization on the growth of crayfish tonic and phasic motor axons in culture.

Previous studies have demonstrated neuron-specific differences in the inhibitory effects of depolarization upon neurite outgrowth. We examined whether there is a relationship between the normal impulse activity level of an axon and the effect of depolarization upon its growth. Inactive phasic motor axons and active tonic motor axons grow from crayfish abdominal nerve cord explants in culture. Depolarization of these axons with high K solutions produced greater inhibition of advancing growth cones from the phasic axons than from the tonic axons. During the period 20-40 min after the beginning of depolarization, tonic axon growth cones continued to advance, whereas phasic axon growth cones retracted. During chronic depolarization, all of the phasic axons retracted during the first day and approximately half of the phasic axons had degenerated after 4 days of depolarization. The majority of tonic axons continue to grow after 3 days of depolarization, and all of the tonic axon growth survived the 4 days of depolarization. The different responses of the growing phasic and tonic axons to depolarization appear to be Ca2+ dependent. The inhibitory effects of depolarization upon phasic axon growth were reduced by the Ca2+ channel blockers La3+ and Mg2+. Application of a Ca2+ ionophore, A23187, produces greater inhibition of phasic axon growth than tonic axon growth. This study demonstrates that depolarization produces greater inhibition of growth from inactive motor axons than from active motor axons. This is likely due to differences in Ca2+ regulation and/or sensitivity to intracellular Ca2+.