Viagra slows the visual response to flicker.
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Cyclic Nucleotide Phosphodiesterases, Type 6↗
Biomedical subjects
Andrew Stockman
Publications and source records attributed to Andrew Stockman.
Into the twilight zone: the complexities of mesopic vision and luminous efficiency.
Of all the functions that define visual performance, the mesopic luminous efficiency function is probably the most complex and hardest to standardise or model. Complexities arise because of the substantial and often rapid visual changes that accompany the transition from scotopic to photopic vision. These are caused not only by the switch from rod to cone photoreceptors, but also by switches between different post-receptoral pathways through which the rod and cone signals are transmitted. In this review, we list several of the complexities of mesopic vision, such as rod-cone interactions, rod saturation, mixed photoreceptor spectral sensitivities, different rod and cone retinal distributions, and the changes in the spatial properties of the visual system as it changes from rod- to cone-mediated. Our main focus, however, is the enormous and often neglected temporal changes that occur in the mesopic range and their effect on luminous efficiency. Even before the transition from rod to cone vision is complete, a transition occurs within the rod system itself from a sluggish, sensitive post-receptoral pathway to a faster, less sensitive pathway. As a consequence of these complexities, any measure of mesopic performance will depend not only on the illumination level, but also on the spectral content of the stimuli used to probe performance, their retinal location, their spatial frequency content, and their temporal frequency content. All these should be considered when attempting to derive (or to apply) a luminous efficiency function for mesopic vision.
Adaptation, Ocular↗
A luminous efficiency function, V*(lambda), for daylight adaptation.
We propose a new luminosity function, V*(lambda), that improves upon the original CIE 1924 V(lambda) function and its modification by D. B. Judd (1951) and J. J. Vos (1978), while being consistent with a linear combination of the A. Stockman & L. T. Sharpe (2000) long-wavelength-sensitive (L) and middle-wavelength-sensitive (M) cone fundamentals. It is based on experimentally determined 25 Hz, 2 degrees diameter, heterochromatic (minimum) flicker photometric data obtained from 40 observers (35 males, 5 females) of known genotype, 22 with the serine variant L(ser180), 16 with the alanine L(ala180) variant, and 2 with both variants of the L-cone photopigment. The matches, from 425 to 675 nm in 5-nm steps, were made on a 3 log troland xenon white (correlated color temperature of 5586 K but tritanopically metameric with CIE D65 standard daylight for the Stockman and Sharpe L- and M-cone fundamentals in quantal units) adapting field of 16 degrees angular subtense, relative to a 560-nm standard. Both the reference standard and test lights were kept near flicker threshold so that, in the region of the targets, the total retinal illuminance averaged 3.19 log trolands. The advantages of the new function are as follows: it forms a consistent set with the new proposed CIE cone fundamentals (which are the Stockman & Sharpe 2000 cone fundamentals); it is based solely on flicker photometry, which is the standard method for defining luminance; it corresponds to a central 2 degrees viewing field, for which the basic laws of brightness matching are valid for flicker photometry; its composition of the serine/alanine L-cone pigment polymorphism (58:42) closely matches the reported incidence in the normal population (56:44; Stockman & Sharpe, 1999); and it specifies luminance for a reproducible, standard daylight condition. V*(lambda) is defined as 1.55L(lambda) + M(lambda), where L(lambda) and M(lambda) are the Stockman & Sharpe L- & M-cone (quantal) fundamentals. It is extrapolated to wavelengths shorter than 425 nm and longer than 675 nm using the Stockman & Sharpe cone fundamentals.
Adaptation, Physiological↗
Long-wavelength adaptation reveals slow, spectrally opponent inputs to the human luminance pathway.
In addition to its expected fast, additive L- and M-cone inputs (L + M), the luminance pathway has slow, spectrally opponent inputs. We have previously shown that on long-wavelength fields, the dominant slow signals change from L-M at moderate intensity levels to M-L signals at high. Here, we focus on the transition between them, which we find is marked by substantial changes in temporal phase delay, and by large and unexpected shifts in flicker spectral sensitivity. At moderate temporal frequencies, counter to the selective adaptation caused by the field, spectral sensitivity changes from being M-cone-like to more L-cone-like. These changes can be accounted for by a change in the relative strengths of the slow spectrally opponent cone signals from L-M exceeding M-L below the transition to M-L exceeding L-M above it, and by the resulting changes in constructive and destructive interference between the dominant signal components. We speculate that the transition is caused by the deep-red field becoming equivalent, postreceptorally, to a green field at high bleaching levels. These results further challenge the dogma that there are separable psychophysical channels for the transmission and processing of color and luminance information. Although its output generates an achromatic percept, the luminance channel has spectrally opponent inputs.
Adaptation, Physiological↗
Spectrally opponent inputs to the human luminance pathway: slow +M and -L cone inputs revealed by intense long-wavelength adaptation.
The nature of the inputs to achromatic luminance flicker perception was explored psychophysically by measuring middle- (M-) and long-wavelength-sensitive (L-) cone modulation sensitivities, M- and L-cone phase delays, and spectral sensitivities as a function of temporal frequency. Under intense long-wavelength adaptation, the existence of multiple luminance inputs was revealed by substantial frequency-dependent changes in all three types of measure. Fast (f) and slow (s) M-cone input signals of the same polarity (+sM and +fM) sum at low frequencies, but then destructively interfere near 16 Hz because of the delay between them. In contrast, fast and slow L-cone input signals of opposite polarity (-sL and +fL) cancel at low frequencies, but then constructively interfere near 16 Hz. Although these slow, spectrally opponent luminance inputs (+sM and -sL) would usually be characterized as chromatic, and the fast, non-opponent inputs (+fM and +fL) as achromatic, both contribute to flicker photometric nulls without producing visible colour variation. Although its output produces an achromatic percept, the luminance channel has slow, spectrally opponent inputs in addition to the expected non-opponent ones. Consequently, it is not possible in general to silence this channel with pairs of 'equiluminant' alternating stimuli, since stimuli equated for the non-opponent luminance mechanism (+fM and +fL) may still generate spectrally opponent signals (+sM and +sL).
Adaptation, Physiological↗
Spectrally opponent inputs to the human luminance pathway: slow +L and -M cone inputs revealed by low to moderate long-wavelength adaptation.
The luminance pathway has slow (s), spectrally opponent cone inputs in addition to the expected fast (f), non-opponent inputs. The nature of these inputs to luminance flicker perception was further explored psychophysically by measuring middle- (M-) and long-wavelength-sensitive (L-) cone modulation sensitivities, M- and L-cone phase delays, and flicker spectral sensitivities under three conditions of low to moderate long-wavelength adaptation. Under these conditions we find that the luminance channel has fast M- and L-cone input signals (+fM and +fL), and slow, spectrally opponent cone input signals (+sL and -sM). The slow signals found under these conditions are therefore of the opposite polarity to those (+sM and -sL) found under more intense long-wavelength adaptation. At these less intense levels, fast and slow M-cone signals of opposite polarity (-sM and +fM) cancel at low frequencies, but then constructively interfere at intermediate frequencies (ca 12.5-22.5 Hz, depending on adapting level) because of the delay between them. In contrast, fast and slow L-cone signals of the same polarity (+sL and +fL) sum at low frequencies, but then destructively interfere at intermediate frequencies. Importantly, the spectrally opponent signals (+sL and -sM) contribute to flicker nulls without producing visible colour variation. Although its output generates an achromatic percept, the luminance channel has slow spectrally opponent as well as fast non-opponent inputs.
Adaptation, Physiological↗
Identification of novel RPGR ORF15 mutations in X-linked progressive cone-rod dystrophy (XLCORD) families.
PURPOSE: To test the incidence of mutations in RPGR ORF15 in six families with X-linked progressive retinal degeneration (cone-rod dystrophy [XLCORD], macular or cone dystrophy) and to undertake a detailed phenotypic assessment of families in whom ORF15 mutations were identified. METHODS: To amplify and sequence ORF15 in its entirety, a cloning strategy was developed. Families with mutations in ORF15 underwent electrophysiological testing, color vision assessment, color fundus photography, and fundus autofluorescence (AF) imaging. RESULTS: Novel protein truncation mutations were identified in two families. In family A, a 2-bp mutation was identified in ORF15+A1094C G1095T, predicted to result in a truncated protein (E364D/E365X). In family B, a G-to-T transversion (ORF15+1176G>T) resulted in a nonsense mutation (G392X). Characteristics of phenotype in both families included progressive deterioration of central vision and subsequently night vision, mild photophobia, and moderate to high myopia. Ophthalmoscopic abnormalities were generally confined to the macula. A parafoveal ring of increased AF was observed, and electrophysiological evidence of a greater generalized abnormality in cone than rod responses were consistent with a cone-rod dystrophy phenotype. CONCLUSIONS: The cloning strategy for ORF15 facilitated comprehensive sequence analysis in patients. Two families were identified with nonsense mutations, and clinical evaluation revealed them both to have a similar phenotype. The presence of a parafoveal ring of increased AF was an early indicator of affected status in these families. No disease-causing mutations in ORF15 were detected in four other families, suggesting that ORF15 mutations may not be the most common cause of XLCORD.
Adult↗