688 



HANDBOOK OF PHYSIOLOGY ^ NEUROPHYSIOLOG\- I 



—I 1 1 1 1 1 \ 1 



Synthesis of photo pigmerrts 



from chicMen opsins + retinene 



O.S - 



0.4 



03 



2 



0.1 



a - 



I I r 



rhodopsin (SOOm/i ) 



iodopsin fS60mp) 



Time in diarK~nninutas 



A L 



J \ L 



;o 



20 



30 



FIG. 2 1. Synthesis of iodopsin and rhodopsin in solution from a mixture of chicken opsins and 

 neo-i retinene. 23°C. This is the same experiment as shown in figure lo but with the rhodopsin 

 extinctions multiplied by 1.3. At this temperature, iodopsin synthesis is complete within 2 to 3 

 min., whereas rhodopsin synthesis still continues after 35 min. [From W'ald C72).] 



neurons and synapses along the optic pathways — 

 may also play a role. Of this possibility as yet very 

 little is known. In general, nein-al adaptations are 

 relatively rapid; if they enter at all, they should 

 probably be completed during the earliest stages 

 ot visual adaptation. They probabh' are responsible 

 al,so for only a minor portion of the range of \isual 

 adaptation. As a first approximation, light and dark 

 adaptation seem to reflect the fall and rise of visual 

 pigment; and specifically it is the log sensitivity which 

 runs parallel with pigment concentration. 



I iliiiiiiii A Deficiency and .A'lghl Blindness 



Probably the earliest symptom of \-itamin A de- 

 ficiency in man and other animals is the rise of visual 

 threshold known as night blindness. Because night 

 vision is associated with the rods, it was once thought 

 that dietary night blindness, so called to distinguish 

 it from the idiopathic or congenital disease, is a 

 failure specifically of rod \ision. The first experi- 

 mental studies of human night blindness, however, 

 showed at once that in \itamin A deficiency cone 

 vision deteriorates with rod \ision, and both recover 

 together on administration of \itamin A (figs. 22, 23) 

 (26, 27, 77). 



The realization that both iodopsin and rhodopsin 

 are synthesized from the same form of vitamin .\ 

 oflfers a substantial theoretical basis for this relation- 

 ship. To he sure, iodopsin has not been demonstrated 

 in human cones; if present, it is presumably ac- 

 companied by at least two other cone pigments 

 needed to account for normal human color vision. 

 \'et the observation that on administration of \itamin 

 .■\, or carotene, night blindness is repaired as quickly 

 and completely in the cones as in the rods (fig. 23) 

 implies that the human cone pigments as a group 

 are probabh' synthesized from vitamin A. Just as 

 rhodopsin and iodopsin are constructed by joining 

 the same prosthetic group to different opsins, so the 

 cone pigments responsible for human color vision 

 may well be composed of the same retinene com- 

 bined with a variety of different opsins. 



The opsins ha\e been altogether a neglected coiti- 

 poncnt in the etiology of dietary night blindness. 

 This disease and its cure have been thought of too 

 much in terms of the removal and replacement of 

 \itamin A, particularly since vitamin A was shown 

 to be a precursor of rhodopsin. This preconception 

 may be the source of some of the embarrassments 

 that have attended the experimental study of night 

 blindness: a) on beginning a vitamin A-deficienl 



