DARK ADAPTATION 77 



Then, too, a part of dark-adaptation — it is hard to say how much — is 

 accompUshed by switchboard effects in the integrative layers of the 

 retina, bringing about temporary hook-ups, to gangUon cells, of larger 

 numbers of visual cells than usual. 



In dim light or darkness, the destruction of rhodopsin having largely 

 or wholly ceased, the new formation of the substance (partly from the 

 decomposition products still present in the rods, partly from new raw 

 material absorbed from the pigment epithelium) quickly restores the 

 concentration to a fairly high level. Within seven or eight minutes, in 

 fact, the previously depleted rod becomes capable of function. The rods 

 are now deeply colored and absorb much more of whatever light may 

 strike them, so that a strong impulse impinges upon the bipolar. Should 

 we now emerge into a bright place, the light would dazzle us uncomfort- 

 ably until enough rhodopsin had been destroyed to raise the thresholds 

 of the rods considerably. This process takes a much larger fraction of 

 a second than is required for the pupil to constrict. So, the removal of 

 some of the rhodopsin is the controlling factor in /zg/?/-adaptation — 

 which we might loosely define as the destruction of excessive sensitivity. 

 The pupil slowly reopens as the sensitivity of the retina is decreased, and 

 attains a final 'physiological size' appropriate to the particular species of 

 animal, and which for man is maintained in all intensities between 100 

 and lOOOlux — the range within which, presumably, an equilibrium can 

 be maintained in the photochemical system of the visual cells. 



Rhodopsin accumulates to a considerable proportion of its maximum 

 in half an hour and is almost at maximum in an hour; but it continues 

 to form slowly for twenty-four hours or more. If anything essential for 

 its manufacture is deficient in the individual or in his diet, the rate of 

 formation will be greatly retarded, and the greatest amount ever formed 

 will be much less than normal. This condition of deficiency leads to 

 nyctalopia or night-blindness, in which dark-adaptation is incomplete 

 and the individual feels the handicap when trying to make his way about 

 in dim places and at night. He may become a menace to his fellows if 

 he drives an automobile at night and meets many bright headlights 

 which assault the little rhodopsin he is able to form. In the armies of 

 years ago, night-blindness — common under conditions of malnutrition — 

 automatically exempted a soldier from nocturnal guard duty. In modern 

 warfare, the night-blind individual is particularly useless in defense 

 against nocturnal bombing, and every effort is made to maintain a high 

 concentration of rhodopsin in the retinae of night fighter aircraftsmen. 



