436 



ANNALS NEW YORK ACADEMY OF SCIENCES 



similar time-course may be assumed for the current penetrating the 

 closely adjacent post-synaptic membrane (see figure 5). The first 

 derivative of the monophasic potential gives, of course, the expected 

 diphasic effect, A1C2. 



Thus, it may be concluded that, so far as they go, ephaptic investi- 

 gations lend support to the hypothesis that an excitatory action would 

 be exerted by impulses terminating at synapses. However, with 

 ephapses, this excitatory action is normally too weak to initiate im- 

 pulses in the resting fiber. For example, Katz and Schmitt*^ find that 

 the maximum C effect is never as much as 20% of threshold, and 

 Arvanitaki^ has to sensitize the resting fiber by decalcification, in 

 order to increase the local response sufficiently for impulse initiation.* 



/ 



T^ 



\^ ^ 



/ 



(a) 



(b) 



Figure 5. Diagrams of current flow at a schematic synapse with pre-synaptic impulse ap- 

 proaching synapse in (a), and at synapse in (b). Note reversal of current flow, the focal Ai 

 effect being followed by the focal C2 effect at the synaptic region of the post-synaptic membrane. 



The Hering effect, ephaptic transmission adjacent to killed or injured 

 regions,^^' *^' " may also be explained as due to A1C2 stimulation of 

 fibers rendered sensitive by the catelectrotonus'* prevailing close to the 

 injured region. Tests of excitability changes, 4 ram. from the killed 



* Cf . Arvanitaki, A.> Figure S. 



