Sodium channels in the axolemma of normal and degenerating rabbit optic nerve.
Section of a rabbit peripheral nerve leads to axonal degeneration and a proliferation of Schwann cells, and it is known to lead to a profound increase in the saxitoxin binding capacity of its distal portion, suggesting that Schwann cells may bind this marker for sodium channels. The present study shows, however, that crush with subsequent axonal degeneration of the central axons of the rabbit optic nerve leads to a slow monotonic fall in the saxitoxin binding capacity, which by 100 days after crush is not significantly different from zero. This suggests that central glial cells (astrocytes and oligodendrocytes) do not bind saxitoxin, and that the saturable binding of saxitoxin to this nerve is entirely to the axolemma. On this basis, the value for total saxitoxin binding capacity of the normal rabbit optic nerve, taken together with the morphometric data of D. I. Vaney & A. Hughes (J. comp. Neurol. 80, 241-252 (1976)), yields a sodium channel density of about 400-700 channels per square micrometre nodal axolemma.
D000818:Animals; D001369:Axons / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism; D009410:Nerve Degeneration; D009457:Neuroglia / Q000378:metabolism; D009900:Optic Nerve / Q000378:metabolism*; D011817:Rabbits; D012530:Saxitoxin / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*
D007473:Ion Channels; D012530:Saxitoxin; D012964:Sodium