Facilitation of sodium currents in frog neuroglia by nerve impulses: dependence on external calcium.
Facilitation of voltage-gated sodium currents in glial membranes by nerve impulses has been studied by using both the whole cell and loose-patch clamp techniques in the isolated intact optic nerve of the frog. During facilitation there is a shift in the voltage dependence of glial Na+ channels such that a given depolarization produces a larger inward Na+ current. Decreasing external calcium from 4 times normal to 0.2 times normal produced a similar shift in the current-voltage relation. Increasing the external calcium concentration to 4-5 times normal blocks facilitation. In reduced calcium, 0.1-0.2 times normal, the peak of facilitation was unaffected, but its decay was slowed. The addition of 1 mM nickel and 2 mM cobalt or 2 mM cadmium, to prevent depletion of extracellular calcium that might result from voltage-dependent entry of calcium into the axons, did not block the facilitation. The results suggest that, even though facilitation is blocked by high extracellular calcium, a decrease in extracellular calcium produced by axon impulses is not the cause of the facilitation.
Marrero
H
H
Institute of Neurobiology, University of Puerto Rico, San Juan 00901.
Orkand
R K
RK
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D003035:Cobalt / Q000494:pharmacology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009457:Neuroglia / Q000187:drug effects / Q000502:physiology*; D009532:Nickel / Q000494:pharmacology; D009900:Optic Nerve / Q000502:physiology*; D011894:Rana pipiens; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*
D015222:Sodium Channels; D003035:Cobalt; D009532:Nickel; D002118:Calcium