Abstract

Analysis of spectral response peaks shows that receptor curves can hardly be deduced by psychophysics or nerve physiology. Conversely, however, even the two known dyes may suffice for all the spectral response peaks, narrow or wide. The detailed structure of the receptor is basis for a masking mechanism which accounts for 3 absorptions, peaked near 510, 540, and 620 mμ. From these, synaptic mechanisms can produce 4 color primaries at the bipolar level, and 6 selectivities at the fiber level. The synaptic detail for this (based on Polyak, Willmer, Müller, and Adams) separates white, and provides for dichromasies, unitary hues, saturation, and nonlinearity of color-limens.

By such mechanism, color antagonists may be transmitted by simple modulation of a mean frequency. Transmission has only a transient appearance, due to a series of electrochemical counter-effects which give minimal signal for steady-state information. Amacrine cells and retinal polarizations apparently relate to this, and thereby constancy and lateral induction of black and hue. Acuity in continuous illumination, in a system which transmits mainly transients, is handled by a scanning system. Other counterparts to color television are discussed.

© 1951 Optical Society of America

Full Article  |  PDF Article

Corrections

S. A. Talbot, "Errata," J. Opt. Soc. Am. 42, 989_1-989 (1952)
https://www.osapublishing.org/josa/abstract.cfm?uri=josa-42-12-989_1

References

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L. Sloan, Am. J. Ophthalmol. 30, 705 (1947).
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W. Pitts and W. McColloch, Bull. Math. Biophys. 9, 127 (1947).
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1946 (4)

J. Ten Doesschate, Ophthalmol. 112, 1 (1946).
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J. D. Saunderson and B. I. Milner, J. Opt. Soc. Am. 36, 36 (1946).
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H. A. Van der Velden, Ophthalmol. 111, 321 (1946).
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A. F. Bliss, J. Gen. Physiol. 29, 277 (1946).

1945 (1)

R. B. Morison and D. L. Bassett, J. Neurophysiol. 8, 309 (1945).

1944 (5)

R. Granit, J. Physiol. 103, 103 (1944).

G. M. Byram, J. Opt. Soc. Am. 34, 718 (1944).
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W. S. Stiles, Nature 154, 290 (1944).
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F. H. G. Pitt, Proc. Roy. Soc. (London) B. 132, 101 (1944).
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C. B. Anfinson, J. Biol. Chem. 152, 267 (1944).

1943 (2)

1942 (9)

S. Hecht, J. Opt. Soc. Am. 32, 42 (1942); M. H. PirenneNature 161, 724 (1947).
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C. G. Bernhard, Acta. Physiol. Scand. 3, 301 (1942); J. Neurophysiol. 5, 32 (1942).
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W. H. Marshall and S. A. Talbot, Biol. Sympos. 7, 117 (1942).

J. C. Peskin, J. Gen. Physiol. 26, 26 (1942).

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W. E. L. Clark, Physiol. Rev. 22, 205 (1942).

1941 (5)

R. Granit, Acta Physiol. Scand. 3, 137 (1941).
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D. P. C. Lloyd, J. Neurophysiol. 4, 184 (1941).

D. B. Judd, Am. J. Psych. 54, 289 (1941).
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J. R. Toman, J. Neurophysiol. 4, 51 (1941).

S. A. Talbot and W. H. Marshall, Am. T. Ophthalmol. 24, 1255 (1941).

1940 (7)

S. A. Talbot, Am. J. Physiol. 129, 478 (1940).

F. H. Lewy and G. D. Gammon, T. Neurophysiol. 3, 388 (1940).

Broda, Goodeve, and Lythgoe, J. Physiol. 98, 397 (1940).

L. E. R. Picken, Biol. Rev. 14, 146 (1940).

F. Weigert and J. W. Morton, Ophthalmol. 99, 145 (1940).
[Crossref]

A. Dresler, Das Licht 10, 79 (1940).

R. J. Lythgoe, Br. J. Ophthalmol. 24, 21 (1940).

1939 (6)

J. S. Preston, Proc. Phys. Soc. (London) 51, 757 (1939).
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F. O. Schmitt and R. S. Bear, Biol. Rev. 14, 27 (1939).
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A. Magitot, Traite d’Ophthalmol. 2, 484 (1939).

F. N. Willmer, Doc. Ophthalmol. 3, 194 (1939).
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J. Hecht and E. D. Mintz, J. Gen. Physiol. 22, 593 (1939).

J. F. Schouten and L. S. Ornstein, J. Opt. Soc. Am. 29, 168 (1939).
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1938 (6)

W. D. Wright and R. Granit, Brit. T. Ophthalmol. Suppl. 9, 80 (1938).

W. D. Wright and R. Granit, Brit. J. Ophthalmol. Supp. 9, (1938).

R. J. Lythgoe, Proc. Phys. Soc. (London) 50, 321 (1938).
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W. J. Schmidt, Kolloid-Z. 85, 137 (1938).
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P. Karrer, Doc. Ophthalmol. 1, 259 (1938).

R. Granit, Doc. Ophthalmol. 1, 7 (1938).

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L. E. Gilson, Chem. Abstracts 31, 1830 (1937).

W. J. Schmidt, Protoplasma Monographien 11, 388 (1937).

R. Granit and R. Munsterhelm, J. Physiol. 88, 436 (1937).

1936 (1)

J. P. Bartz and F. O. Schmitt, Am. J. Physiol. 177, 280 (1936).

1935 (1)

G. Osterberg, Acta Ophthalmol. 13, Suppl. 6 (1935).

1933 (2)

G. H. Bishop, Am. J. Physiol. 106, 460 (1933).

H. E. Roaf, Physiol. Rev. 13, 43 (1933).

1932 (2)

J. Guild, “Discussion on Vision,” Phys. Soc. (London), p. 85 (1932).

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1931 (2)

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V. O. Siven, Z. Psychol. Physiol. Sinnesorg 42, 224 (1908).

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[Crossref]

Proc. Roy. Soc. (London) B. (1)

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[Crossref]

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[Crossref]

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Figures (9)

Fig. 12–1
Fig. 12–1

Lamellar structure of receptor’s outer member. L=Lipid layer. P=Protein layer with photodye. a=Interface mainly depolarized by light. b=Interface driving external stimulating current.

Fig. 13–1
Fig. 13–1

Electric responses of retina. A. Frequency at receptor. B. At optic nerve. C. Components of electric polarization (Fig. 15–1).

Fig. 13–2
Fig. 13–2

Dominators and modulators of an Adams-Müller model. B, G, Y, R fundamentals. R580R610=Yfoveal. 8, 7, 6 same, brought to equal max ordinate (Dominators). 4, 3, 2, 1 same, subtracted by pairs (fig. 15–2B) (Modulators).

Fig. 13–3
Fig. 13–3

Modulators found at optic-nerve level (range limits) after: Granit, reference 19.

Fig. 13–4
Fig. 13–4

Dominators and modulators from neurophysiology after: Granit, reference 19.

Fig. 15–1
Fig. 15–1

Neural model of modified Adams-Müller retina. Cell polarization: α(l), β(m, p), γ(defh), δ(a, b) Y570=aG540+bR610; dZ forms B hump on R. Hachures show deficiencies.

Fig. 15–2A
Fig. 15–2A

Primaries of a modified Adams-Müller system B, G, R580 processes from König, Ladd-Franklin. B=d-bipolar response. G=e-cell response. Y=e-f-cell response. R=(dZ+f) response. 2B: r(g)=RG: p-response, normal and protanopic. y(b)=YB: m-fiber response, normal and protanopic.

Fig. 15–4
Fig. 15–4

Coordinates of r(g) and y(b) in Adams’ x ¯ z ¯ plane of equal luminosity. YB zero at w, RG zero at y.

Fig. 15–5
Fig. 15–5

Photochemical range vs neural range above null (“brighter”) yields r, y, white chroma below null (“darker”) yields g, b, black chroma note shift of null with higher adaptive state.

Tables (1)

Tables Icon

Table 15–3 Operations in normal and reduced retinal mechanism.