HIGH ENERGY IRRADIATION: BIOELECTRIC EFFECTS 293 



tory p)eriod of a nerve is the time element required to restore the helical 

 macromolecule to the constrained state. 



Hodgkin and Katz (1949) have presented evidence show^ing that at rest 

 the ionic permeability of potassium is 25 times that of sodium. During 

 excitation these ionic permeabilities are quickly reversed, so that sodium is 

 25 times as permeable as potassium. The burden of accounting for this 

 sudden ionic shift has undone many an ingenious membrane hyp>othesis. The 

 cocked-uncocked f>erformance of helical molecules in the present membrane 

 model supplies an adequate explanation not only for the permeability events 

 triggered by excitation, but also for the time constants for the limbs of the 

 action potential. 



The character of the cocked protein molecule is such as to allow for a 

 rapid change to the relaxed structural state, thus accounting for the fast 

 time constant of the ascending limb of the action potential. To "reconstrain" 

 the relaxed helical macromolecules suggests a need for an energy input. 

 Since the ratio of heat produced during activity over that produced in re- 

 covery shows that the latter requires most of the energy, we have another 

 observation that does not violate the model, but agrees with it. 



Developing a membrane model has made the task of interpreting how 

 radiation energy influences neural functioning, relatively easy. Only an 

 average energy of some tens of electron volts can be accepted by a molecule. 

 Successive energy transfers occurring along the path of high energy particles 

 (kinetic energies in the thousand or million electron volt range) supersede 

 the acceptable energy level, and a defective molecule is the consequence. For 

 conducting axons, it is construed that the most radiation-labile molecules are 

 the membrane protein macromolecules. When the structure of these mole- 

 cules is damaged, excitability is affected. 



Radioactive tracer studies of resting nerve (Rothenburg, 1950; also see 

 Radioactive Studies in this paper) reveal that radiation causes an increase 

 in sodium ion permeability, i.e., a shift in the mode channel size from potas- 

 sium toward sodium (see Fig. 13, resting state versus irradiation state). 

 Bioelectric studies on single myelinated nerve fibers after irradiation (Gaffey, 

 1960) indicate that there is an increase in potassium ion permeability 

 (revealed by a decrease in the slope of the falling limb of the action poten- 

 tial) and a decrease in sodium ion pemieability (connoted by a decrease in 

 the slope of the rising limb of the action potential). The deterioration of 

 selective ion permeability in the conducting nerve is viewed as a translation 

 in the mode channel size from sodium toward potassium (Fig. 13, conduct- 

 ing state versus irradiation state). These early signs of neural impairment 

 would be expected as a consequence of the partial loss of the ability of the 

 helical molecules of the membrane to fully coil-uncoil. The terminal degener- 



