INHIBITORY INTERACTION IN THE RETINA 251 



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Fig. 9. After-discharge from an ommatidium inhibited by illumination of a nearby 

 retinal region (bottom record); control {top record) for comparison. The after- 

 discharges were elicited by intense illumination of the ommatidium for several 

 seconds, ending just before the beginning of each record. Illumination of nearby 

 region signalled by blackening of white band above time marks. Time in ' sec. 



proximally in the optic nerve; hence it is not the resuU of a dropping out of 

 impulses as the fibers traverse the plexus. 



We have some preliminary observations on a change in membrane potential 

 of impaled eccentric cells inhibited by illuinination of adjacent ommatidia. 

 E. F. MacNichol found, in the case of an ommatidium that was spontaneously 

 active and unresponsive to light, that on illumination of neighboring omma- 

 tidia, the spontaneous activity was slowed concomitantly with a small hyper- 

 polarization of the eccentric cell membrane (personal communication). We 

 have found that preparations showing no signs of injury (no spontaneous 

 activity and unimpaired sensitivity to light) also show hyperpolarization con- 

 comitant with a slowing of the discharge of impulses. In the record shown in 

 Fig. 10 (obtained in collaboration with F. A. Dodge) a constant frequency of 

 spike discharge was maintained by passing a small depolarizing current 

 through the recording pipette. An impulse occurred just before the start of 

 the record. At the first arrow neighboring ommatidia were illuminated, taking 

 care to prevent scattered light from stimulating the test ommatidium. After 

 a short latency the basehne showed a negative deflection. The illumination 

 was discontinued at the second arrow, whereupon the membrane potential 

 returned to the firing level and the spike discharge was resumed. The fact that, 

 during inhibition of slightly depolarized cells, the membrane potential tended 

 towards the resting potential would seem to indicate a synaptic inhibitory 

 mechanism similar to that of other preparations which have been analyzed 

 more extensively (Fatt and Katz, 1953; Brock et al., 1952; Kuffler and 

 Eyzaguirre, 1955). 



Even though we do not have a clear understanding of the cellular mech- 

 anisms of the inhibitory interaction, it is stifl possible to understand its conse- 

 quences as a basis of an integrative mechanism in the eye. We begin our dis- 



