A voltage- and time-dependent rectification in rat dorsal spinal root axons.
1. Rat dorsal spinal roots were studied by the use of whole-nerve sucrose gap and intra-axonal recording techniques. A prominent time-dependent conductance increase as evidenced by a relaxation or "sag" in membrane potential toward resting potential was elicited in dorsal spinal roots by constant hyperpolarizing current pulses. The relaxation, or sag, indicative of inward rectification, reached a maximal level and then decayed during the current pulse. 2. The time-dependent sag elicited by hyperpolarization was reduced when Na+ or K+ was removed from the normal bath solution but was abolished with the removal of both Na+ and K+. Tetrodotoxin (TTX), tetraethylammonium (TEA), and 4-aminopyridine (4-AP) did not affect the depolarization sag, suggesting that conventional voltage-dependent sodium and potassium channels do not underlie the inward rectification. 3. Cs+ in low concentrations completely abolished the inward rectification, whereas Ba2+ induced a partial block. 4. Current-voltage curves indicate that the magnitude of the depolarizing sag increases monotonically with increasing hyperpolarization. The time required to reach peak hyperpolarization, maximal sag potential, and the time between peak hyperpolarization and sag membrane potentials decreases with increasing levels of hyperpolarization. 5. The inward rectification is refractory to further stimulation during its decay phase, as revealed by paired-pulse protocols. This decay in inward rectification is both time and voltage dependent and is observed on a single axon level by the use of intra-axonal recording techniques as well as from whole-root recordings in the sucrose gap. 6. It is concluded that rat dorsal root fibers display a prominent time-dependent conductance increase in response to hyperpolarization that depends on both Na+ and K+ permeability and is blocked by Cs+. This rectification displays a decay phase that has not been previously described for similar conductances. It is argued that the Na+ component of this conductance is primarily responsible for stabilizing membrane potential near resting potential during periods of hyperpolarization.
Birch
B D
BD
Department of Neurology, Yale University School of Medicine, New Haven 06510.
Kocsis
J D
JD
Di Gregorio
F
F
Bhisitkul
R B
RB
Waxman
S G
SG
D000818:Animals; D001369:Axons / Q000502:physiology*; D001464:Barium / Q000494:pharmacology; D002586:Cesium / Q000494:pharmacology; D004558:Electric Stimulation; D004594:Electrophysiology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D008839:Microelectrodes; D011188:Potassium / Q000502:physiology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012032:Refractory Period, Electrophysiological / Q000187:drug effects; D012964:Sodium / Q000502:physiology; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology; D013126:Spinal Nerve Roots / Q000502:physiology*; D013997:Time Factors
D015221:Potassium Channels; D015222:Sodium Channels; D002586:Cesium; D001464:Barium; D012964:Sodium; D011188:Potassium