The requirement for calcium ions and the effect of other ions on axoplasmic transport in mammalian nerve.

Abstract

Until recently it was believed axoplasmic transport in vitro was not affected by Ca2+, with normal transport in Ca2+-free medium. This was due to the presence of the relatively impermeable perineurial sheath around the nerve trunks. Using a desheathed cat peroneal nerve preparation, axoplasmic transport required an adequate level of Ca2+ in the external medium. In a buffered Ca2+-free medium, transport began to decline within 30 min and a complete block occurred in 2.6 h. A 5 mM-Ca2+ concentration added to a buffered isotonic sucrose or NaCl solution was able to maintain transport. With lower Ca2+ concentrations of 1.5-3.0 mM, usually present in the extracellular fluid or in a Ringer medium, some trnasport impairment occurred but the addition of 4 mM-K+ restored the normal axoplasmic transport pattern. With Ca2+ concentrations below 0.75 mM 4 mM-K+ was unable to sustain transport. K+ alone at a concentration of 4 mM when added to a buffered isotonic sucrose or NaCl medium was unable to prolong the time of transport block beyond that in buffered isotonic NaCl or sucrose solutions. In K+ concentrations up to 25 mM, 1.5-5 mM-Ca2+ was required for normal transport. With moderately higher K+ concentrations in the range of 50-100 mM, normal appearing transport was seen with or without Ca2+. This occurred whether or not Na+ was present in the medium. At higher K+ levels, 120-150 mM, decreased transport was seen, with or without the addition of 15 mM-Na+ or Ca2+ in concentrations of 1.5-3.0 mM. Although Mg2+ could not substitute completely for Ca2+ in maintaining transport, it prolonged the time before block occurred. An extra 30-60 min of downflow was seen when 5 mM-Mg2+ was added to a buffered isotonic NaCl medium. Mg2+ acts synergistically with Ca2+. Ca2+ concentration as low as 0.25 mM, with the addition of 1.5 mM-Mg2+, was able to maintain transport. The mechanism of Ca2+ regulation occurring in giant nerve fibers and other cells controlling the level of free Ca2+ were considered. The relationship of Ca2+ to the mechanism of axoplasmic transport in nerve fibers is discussed.