title: Ion transport and membrane potential in CNS myelinated axons I. Normoxic conditions.
abstract: Compound resting membrane potential was recorded by the grease gap technique during normoxic conditions (37 degrees C) in rat optic nerve, a representative CNS myelinated tract. Mean potential was -47 +/- 3 (SD) mV and remained stable for 2-3 h. Input impedance of a single optic nerve axon was calculated to be approximately 5 Gomega. Contribution of the Na+ pump to resting axonal potential is estimated at -7 mV. Ouabain (10 microM to 10 mM) evoked a dose-dependent depolarization that was maximal at >/=1 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 tetrodotoxin (TTX; 1 microM) alone, indicating both TTX-sensitive and -insensitive Na+ influx pathways in resting rat optic nerve axons. Resting probability (P)K: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.
authors.affiliation: Loeb Research Institute, Ottawa Civic Hospital, University of Ottawa, Ottawa, Ontario K1Y 4E9, Canada.
authors.forename: L
authors.initials: L
authors.lastname: Leppanen
authors.forename: P K
authors.initials: PK
authors.lastname: Stys
mesh_terms: D000818:Animals; D001369:Axons / Q000502:physiology*; D002490:Central Nervous System / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D017136:Ion Transport / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology*; D009186:Myelin Sheath / Q000502:physiology; D009900:Optic Nerve / Q000502:physiology; D010042:Ouabain / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000378:metabolism
chemical_list: D004791:Enzyme Inhibitors; D010042:Ouabain; D012964:Sodium