FREDERICK CRESCITELLI 179 



depolarization of bullfrog nerve fibers. While experiments with sodium- 

 deficient solutions were not listed by Lundberg he did include experiments 

 with sodium at twice the normal concentration which were interpreted as 

 indicating an inhibition of the potassium depolarization. He also reported 

 that the conduction block by excess potassium could be greatly delayed 

 by increasing the sodium concentration. There is one great difficulty in 

 utilizing Lundberg's data in an interpretation of the accelerated potassium 

 block in the presence of deficient sodium (fig. 2). TMA was employed as 

 an osmotic substitute in the experiments of figure 2. Lundberg reported 

 that this organic cation was capable of inhibiting posassium depolorization 

 to a degree even greater than sodium. In terms of Lundberg's results the 

 combination of T]\IA and sodium in the present experiments should have 

 been at least as equally effective as 110 niM NaCl in inhibiting depolariza- 

 tion by potassium and slowing down the rate of block. Since this was not the 

 outcome of these experiments there is either some unaccountable factor in 

 one of these investigations or else a simple explanation in terms of depolari- 

 zation is insufficient at these low sodium levels. The experiment of figure 2 

 also suggests a rather interesting difference in temporal action on the 

 part of sodium and potassium ions. This is especially well shown for the 

 A fibers in the step which employed NaCl at a concentration of 11 min. 

 This solution, though unable to maintain activity in any of the A fibers, 

 was nevertheless able to bring about a significant transient recovery in 

 many of them. The action of potasium in causing secondary block must 

 have been delayed in relation to the action of sodium in relieving the low 

 sodium block. 



ACTION POTENTIALS AT LOW TEMPER.\TURE 



When an isolated nerve preparation, mounted on its electrodes within 

 a moist air chamber, was transferred from a normal temperature of about 

 23°G to a low temperature (5°C or less) a progressive change in height of 

 the compound spike was recorded. The detailed changes were slightly 

 different, in a quantitative sense, for difTerent nerve preparations but 

 the important features are adequately emphasized in figure 3. The data 

 obtained with the sheathed nerve (fig. 3) will serve to illustrate the pro- 

 cedure which was followed. The nerve, after dissection, was placed in 

 position on the electrodes in the moist chamber in a constant temperature 

 water bath at 23.5°C. After allowing a period for equilibration the mono- 

 phasic A compound spike was recorded employing as a stimulus a shock 

 at three times the strength required to elicit maximal A activity. The 

 nerve within its chamber was next transferred to a second water l)ath 

 operating at 2.2°C. The first record obtained in about a minute after this 

 transfer was almost identical in height to the response obtained at 23.5°C. 



