Compound action potential (CAP) conduction and Na+ channel content were studied in optic nerves from control and myelin-deficient (md) rats. Action potential propagation was approximately five times slower in the md rat, but the action potentials propagated securely and had frequency-following and refractory properties equivalent to control myelinated axons. Tritium-labelled saxitoxin ([3H]-STX) binding in md optic nerve was approximately 30% greater, per wet mass of tissue, than in the control optic nerve. However, calculations of channel density per axon based on previously published anatomical data from md and control optic nerves (Dentinger et al. 1985) show an equivalent number of sodium channels per axon, with an average density of 10 channels micron-2 in md and 11 channels micron-2 in control optic nerve axons. The amplitude of the CAP in both control and md optic nerves was significantly attenuated by 50 nM TTX, precluding the possibility that TTX-insensitive channels are responsible for the action potential in myelinated or amyelinated axons. In addition, the amplitudes of voltage-activated Na+ currents in type I and type II astrocytes cultured from control and md optic nerves were similar, suggesting that the glial component of Na+ channels is not abnormal in the optic nerve of the md rat. These results suggest that myelination (or its absence) may not directly regulate the number of axonal Na+ channels.