ACTION-POTENTIAL CONDUCTION AND SODIUM-CHANNEL CONTENT IN THE OPTIC-NERVE OF THE MYELIN-DEFICIENT RAT

Compound action potential (CAP) conduction and Na+ channel content wer e studied in optic nerves from control and myelin-deficient (md) rats. Action potential propagation was approximately five times slower in t he md rat, but the action potentials propagated securely and had frequ ency-following and refractory properties equivalent to control myelina ted axons. Tritium-labelled saxitoxin ([H-3]-STX) binding in md optic nerve was approximately 30% greater, per wet mass of tissue, than in t he control optic nerve. However, calculations of channel density per a xon based on previously published anatomical data from md and control optic nerves (Dentinger et al. 1985) show an equivalent number of sodi um channels per axon, with an average density of 10 channels mu m(-2) in md and 11 channels mu m(-2) in control optic nerve axons. The ampli tude of the CAP in both control and md optic nerves was significantly attenuated by 50 nM TTX, precluding the possibility that TTX-insensiti ve 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 N a+ channels is not abnormal in the optic nerve of the md rat. These re sults suggest that myelination (or its absence) may not directly regul ate the number of axonal Na+ channels.