50 



E. F. MACNICHOL, JR. 



Fig. 15. Inhibition of impulses discharged in single units in the Limulus eye by 

 illumination of neighboring units. The black band above the time trace indicates 

 the duration of the inhibitory illumination. Time marks indicate fifths of a second. 

 (Figure courtesy of H. K. Hartline.) 



turned off then the frequency speeds up to nearly its initial value. The two 

 records were made at different intensities of illumination. That the inhibitory 

 effect is produced by activity of the neural elements rather than by the action 

 of some photochemically liberated substance was shown by Tomita (to be 

 published) who found that antidromic stimulation of the nerve fibers arising 

 from adjacent units would also produce an inhibitory effect. In other words, 

 no light was necessary to produce inhibition; only the activity of adjacent 

 units was required as shown in Fig. 16. 



Histology shows that in the Limulus eye there are no ganglion cells and that 

 there are axonal cross connections. These were shown in Fig. 6. 



The receptor cell is somehow affected by these connections between the 

 axons, since we have found that the inhibitory effect can be picked up just as 

 well as a frequency change by a micropipette inserted into an ommatidium as 

 it can back in the optic nerve. 



It is probable that the inhibitory effect is exerted directly upon the impulse 

 generating mechanism since inhibition is produced upon illumination of nearby 

 elements irrespective of the method of stimulating the active element. We have 

 found that trains of impulses produced by injury, changes in chemical environ- 

 ment, electrical stimulation, or by after-discharge subsequent to intense il- 

 lumination can be inhibited as easily as those produced during direct illumina- 

 tion. 



A tentative hypothesis is that the inhibitory connections exert their effects 

 by altering the state of polarization of the region at which impulses originate. 

 Unfortunately we do not yet know where this region is. There is some evidence 

 that it is in the axon near its junction with the cell body. In the first place the 

 spike potentials recorded from micropipettes are never as great as the resting 

 potential of the receptor cell (resting potential 50 mv.; spikes 25-40 mv.) even 

 when there is no injury discharge and the cell appears to be functioning nor- 

 mally in every way. This would indicate that the impulses never invade the 



