Na+ channel accumulation on axolemma of afferent endings in nerve end neuromas in Apteronotus.
In mammals, cut sensory axons trapped in a nerve end neuroma have been shown to develop hyperexcitability, and to become a source of ectopic afferent discharge and abnormal sensation. We have explored cellular mechanisms underlying neuroma electrogenesis. First we confirmed that ectopic neuroma discharge develops in injured afferents in the electrosensory lateral line nerve of the weakly electric fish Apteronotus, as it does in mammals. Then, using previously characterized antibodies that specifically recognize Na+ channel proteins in this species, we obtained light and electron microscopic evidence of abnormally intense immunolabelling of axolemma at the injury site. Accumulation of excess Na+ channels in afferent endings in neuromas could account for their electrical hyperexcitability.
Devor
M
M
Department of Zoology, Life Sciences Institute, Hebrew University of Jerusalem, Israel.
Keller
C H
CH
Deerinck
T J
TJ
Levinson
S R
SR
Ellisman
M H
MH
D000818:Animals; D001369:Axons / Q000378:metabolism / Q000648:ultrastructure; D002462:Cell Membrane / Q000378:metabolism* / Q000648:ultrastructure; D003714:Denervation; D004555:Electric Fish; D004594:Electrophysiology; D007150:Immunohistochemistry; D008854:Microscopy, Electron; D009186:Myelin Sheath; D009416:Nerve Regeneration; D009463:Neuroma / Q000378:metabolism* / Q000648:ultrastructure; D009475:Neurons, Afferent / Q000378:metabolism* / Q000648:ultrastructure; D015222:Sodium Channels / Q000378:metabolism* / Q000648:ultrastructure
D015222:Sodium Channels