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Noninactivating, tetrodotoxin‐sensitive Na + conductance in peripheral axons
Author(s) -
Tokuno Hajime A.,
Kocsis Jeffery D.,
Waxman Stephen G.
Publication year - 2003
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.10421
Subject(s) - tetrodotoxin , hyperpolarization (physics) , depolarization , biophysics , chemistry , sodium channel , neuroscience , sucrose gap , dorsal root ganglion , anatomy , electrophysiology , biology , dorsum , sodium , organic chemistry , nuclear magnetic resonance spectroscopy
Abstract A noninactivating, persistent sodium current has been demonstrated previously in dorsal root ganglia neurons and in rat optic nerve. We report here that Na + channel blockade with tetrodotoxin (TTX) in isolated dorsal and ventral roots elicits membrane hyperpolarization, suggesting the presence of a persistent Na + current in peripheral axons. We used a modified sucrose‐gap chamber to monitor resting and action potentials and observed a hyperpolarizing shift in the nerve potential of rat dorsal and ventral roots by TTX. The block of transient inward Na + currents was confirmed by the abolition of compound action potentials (CAPs). Moreover, depolarization of nerve roots by elevating extracellular K + concentrations to 40 mM eliminated CAPs but did not significantly alter TTX‐induced hyperpolarizations, indicating that the persistent Na + currents in nerve roots are not voltage‐dependent. Tetrodotoxin‐sensitive persistent inward Na + currents are present in both dorsal and ventral root axons at rest and may contribute to axonal excitability. Muscle Nerve 28: 212–217, 2003