Ion transport and membrane potential in CNS myelinated axons. I: normoxic
conditions
Lisa Leppanen and Peter K. Stys
Loeb Research Institute, Ottawa Civic Hospital, University of Ottawa,
Ottawa, ON Canada K1Y 4E9
APStracts 4:105N, 1997.
ABSTRACT
Compound resting membrane potential was recorded by the grease gap technique
during normoxic conditions (37¡ C) in rat optic nerve, a representative CNS
myelinated tract. Mean potential was -47 ± 3 mV and remained stable for 2-3
hours. Input impedance of a single optic nerve axon was calculated to be Å 5
G½. Contribution of the Na+ pump to resting axonal potential is estimated at -
7 mV. Ouabain (10 µM - 10 mM) evoked a dose-dependent depolarization which was maximal at ³1 mM, depolarizing the nerves to approximately 35-40 % of control
after 60 min. Inhibiting energy metabolism (CN- and iodoacetate) during high-
dose ouabain (1 - 10 mM) exposure caused an additional depolarization,
suggesting additional ATP-dependent, ouabain-insensitive ion transport
systems. Perfusion with zero-Na+ (choline substituted) caused a transient
hyperpolarization, that was greater than with TTX (1 µM) alone, indicating
both TTX-sensitive and insensitive Na+ influx pathways in resting rat optic
nerve axons. Resting PK:PNa is calculated at 20 : 1. In contrast to choline-
substituted solution, Li+-substituted zero-Na+ perfusate caused a rapid
depolarization due to Na+ pump inhibition and the ability of Li+ to permeate
the Na+ channel. TTX reduced, but did not prevent, ouabain- or zero-Na+/Li+ -
induced depolarization. We conclude that the primary Na+ influx path in
resting rat optic nerve axons is the TTX-sensitive Na+ channel, with evidence
for additional TTX-insensitive routes permeable to Na+ and Li+. In addition,
maintenance of membrane potential is critically dependent on continuous Na+
pump activity due to the relatively high exchange of Na+ (via the above
mentioned routes) and K+ across the membrane of resting optic axons.
Received 16 June 1997; accepted in final form 17 June 1997.
APS Manuscript Number J010-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 15 July 1997