1. Until recently it was believed that axoplasmic transport in vitro was not affected by Ca2+, transport being normal in Ca2+-free medium. This was found due to the presence of the relatively impermeable perineurial sheath around the nerve trunks. Using a desheathed cat peroneal nerve preparation, axoplasmic transport was shown to require 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 hr. A concentration of 5 mM-Ca2+ added to a buffered isotonic sucrose of NaCl solution was able to maintain transport. With lower concentrations of Ca2+ of 1 . 5-3 . 0 mM, those usually present in the extracellular fluid or in a Ringer medium, some impairment of transport was seen but the addition of 4 mM-K+ restored the normal pattern of axoplasmic transport. With Ca2+ concentrations below 0 . 75 mM, however, 4 mM-K+ was unable to sustain transport. 2. Potassium by itself at a concentration of 4 mM when added to a buffered isotonic sucrose of NaCl medium was unable to prolong the time of transport block beyond that seen in buffered isotonic NaCl or sucrose solutions. In concentrations of K+ up to 25 mM, 1 . 5-5 mM-Ca2+ was required for normal transport. With moderately higher concentrations of K+ in the range of 50-100 mM, normal appearing transport was seen with or without Ca2+. This was seen whether or not Na+ was present in the medium. At higher levels of K+, 120-150 mM, decreased transport was seen, with or without the addition of either 15 mM-Na+ or Ca2+ in concentrations of 1 . 5-3 . 0 mM. 3. While Mg2+ could not substitute completely for Ca2+ in maintaining transport, it was able to prolong 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. Magnesium also acts synergistically with Ca2+. Concentration of Ca2+ as low as 0 . 25 mM was, with the addition of 1 . 5 mM-Mg2+, able to maintain transport. 4. The results are interpreted in the light of studies of the mechanism of Ca2+ regulation known to occur in giant nerve fibres and other clls controlling the level of free Ca2+. The relationship of Ca2+ to the mechanism considered to underlie axoplasmic transport in nerve fibres is also discussed.
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