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

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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.