EXCITATORY AND INHIBITORY PROCESSES 313 



soma transmission occurs. This effect depends on the depolarizing effect 

 produced by the inhibitory impulses. 



In short, one may have either blocking or enhancing of axon-soma trans- 

 mission during inhibitory activity. The end result depends on a delicate 

 balance between two factors: (1) conductance changes produced at the 

 dendrites by inhibition which will tend to block axo-somatic transmission; 

 and (2) membrane potential changes which the inhibitory impulses are 

 capable of setting up. If the membrane potential change is a depolarization 

 then antidromic invasion will actually be enhanced. This effect is consequently 

 similar to the facilitation of axo-somatic transmission produced by stretch- 

 depolarization of the dendrites (see Fig. 10). 



A difference between facilitation of axo-somatic transmission produced by 

 stretch-depolarization and by inhibitory depolarization is well seen when two 

 antidromic impulses are sent in in close succession. In the first case the first 

 impulse may be fully propagated while the second, riding on top of the 

 after-positivity of the first, is usually blocked (Fig. 10). During inhibitory 

 depolarization a different picture occurs since the after-positivity of the first 

 impulse is wiped out and both antidromic impulses are capable of invading 

 the cell. 



The Ionic Mechanisms Involved in the Inhibitory Process 



In contrast to inhibitory phenomena studied in other structures relatively 

 little information is available concerning the role of different ions in the 

 inhibitory process of crayfish and lobster stretch receptors. 



Fatt and Katz (1953) suggested that inhibition produces appreciable 

 conductance changes on the postsynaptic membrane determined by an 

 increase in permeabihty to K+ and/or CI" across the membrane of the 

 crustacean neuromuscular junction. Boistel and Fatt (1958) later presented 

 evidence indicating that the action of the inhibitory transmitter on crustacean 

 neuromuscular junction is largely dependent on an increase in the permea- 

 bility of CI ions. In spinal motoneurons Coombs et al. (1955) have been 

 able to alter the inhibitory equilibrium level by injections of K+, Cl~, Br~, 

 N0"3, and SCN" ions. In the heart, Harris and Hutter (1956) have been able 

 to show, by the use of K^^, that permeability to this ion is greatly increased 

 during apphcation of acetylcholine and Trautwein and Dudel (1958) have 

 shown that, in the presence of acetylcholine, the equihbrium potential is 

 dependent on the external K+ concentration. 



Evidence for K+ movements during inhibition in the crustacean nerve cells 

 has been reported by Kuffler and Edwards (1958) and by Edwards and 

 Hagiwara (1959). These authors studied the inhibitory potential while 

 changing the K+ content of the bathing solution. They recorded potential 

 changes by means of extracellular electrodes connected to a d.c. amplifier. 



