The ionic permeability of nerve membranes 



axon depolarized by a high external potassium concentration cannot conduct im- 

 pulses, but continues to extrude sodium). It does not follow, however, that this is 

 necessarily true for other tissues. A sodium pump which extruded a stream of Na + 

 ions, like the system in frog skin examined in Ussing's elegant experiments (see 

 Ussing and Zerahn, 1951 ), would make a definite contribution to the resting poten- 

 tial, and such a pump may well be present in mammalian muscle and nerve. There 

 is, indeed, a suggestion of the sort in the recent paper by Bennett, Ware, Dunn and 

 Mclntyre (1953) on the resting potential in mouse muscle fibres in vivo, some of their 

 values being higher than any reasonably attributable to a potassium-diffusion poten- 

 tial. 



It must be appreciated, too, that giant cephalopod axons have an abnormally 

 large ratio of volume to surface, and are hence enabled by their ionic reserves to 

 conduct hundreds of thousands of impulses before any recovery is essential. The situa- 

 tion may be similar in myelinated nerves, in view of their greatly reduced area of 

 active membrane, but is likely to be different in nerve cells having numerous fine 

 dendrites, where the ionic reserves may in effect suffice only for the conduction of a 

 few impulses before they need to be recharged. The marked dependence of the cells 

 of the mammalian central nervous system on a continuous supply of glucose and 

 oxygen is thus not surprising, whether or not they work in precisely the way I have 

 described for non-myelinated invertebrate nerves. 



Two extremely interesting questions about which we are still wholly ignorant are 

 those of the chemical identity of the sodium and potassium carriers, and of the nature 

 of the coupling between them and cellular metabolism. Very few chemical com- 

 pounds are known to be able to discriminate between sodium and potassium as 

 efficiently as the cell membrane, and there is no evidence that any of them are 

 actually found in living cells. The obvious suggestion to make about the link with 

 metabolism is that the sodium pump derives its energy from ATP. This would fit 

 with the facts that in cephalopod axons, which probably have only a small reserve 

 of energy-rich phosphate bonds, the sodium extrusion ceases quite rapidly on inter- 

 ference with metabolism, whereas in frog muscle, which is rich in phosphocreatine, 

 metabolic inhibitors have no very obvious effect on the sodium efflux (Keynes and 

 Maisel, 1954). Moreover Nachmansohn, Coates, Rothenberg and Brown (1946) 

 have presented evidence that ATP and phosphocreatine participate at some point 

 in the discharge of the electric organ. But there is no compelling proof that ATP 

 plays a direct role in driving active transport systems, and we should not ignore the 

 possibility that the fuel consumed by the sodium pump is really some other end- 

 product of metabolism. 



REFERENCES 



Bennett, A. L., Ware, F., Dunn, A. L. and McIntyre, A. R. (1953). The normal 

 membrane resting potential of mammalian skeletal muscle measured in vivo. 

 J. cell. comp. Physiol. 42, 343-357- 



Bernstein, J. (1912). Elektrobiologie. Braunschweig: Vieweg. 



Brink, F., Bronk, D. W., Carlson, F. D. and Connelly, C. M. (1952). The oxygen 

 uptake of active axons. Cold Spr. Harb. Sym. quant. Biol. 17, 53-67. 



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