NERVE ACTIVITY 



tion of electric currents is generally assumed to be as follows: 

 ions are the carriers of electrical currents in living cells. As is 

 today well established, sodium ions are present at a much higher 

 concentration on the outside of nerve and muscle fibers than in- 

 side the cell, and the opposite is true for potassium ions. These 

 concentration gradients are the source of the action potentials 

 and their resulting currents which propagate and are yet part 

 of the impulse. During activity there is an influx of sodium ions 

 (28,29). Apparently owing to a sudden increase in perme- 

 ability, these ions enter the fibers during the rising phase of the 

 action potential (12,14). The influx of sodium ions is followed 

 by an equivalent outflow of potassium ions coinciding essentially 

 with the falling phase. 



Naturally, the question arises, by what mechanism do the 

 ionic concentration gradients, the potential source of EMF, sud- 

 denly become effective? What alterations occur in the mem- 

 brane rendering it more pervious to sodium ions? Knowledge 

 of this process is fundamental for the understanding of the 

 mechanism of generation of the bioelectric currents, that is of 

 conduction. As was postulated by Kurt H. Meyer in 1937, the 

 increased ion permeability must be preceded by a chemical re- 

 action (16). However, the difficulty of identifying this reaction 

 is considerable. The increase in permeability must occur at an 

 extremely high speed, within microseconds, and the barrier must 

 be re-established within a period of time of the order of a milli- 

 second, so that the next impulse may pass again. The studies 

 mentioned above indicate that the acetylcholine system is essen- 

 tial for the nerve impulse and suggest that it is responsible for 

 the alterations of conducting membranes which produce the in- 

 creased ion permeability. The tentative picture which has 

 emerged as to the role of acetylcholine may be briefly outlined 

 (Figure 1). 



Acetylcholine is, in the resting cell, present in an inactive 

 bound form which may be tentatively called the storage form. It 

 appears likely that the ester is bound to a protein or a lipopro- 



633 



