Retinal dark adaptation

After a few minutes illumination ( light-adaptation ) bacteriorhodopsin immobilized in the purple membrane lattice contains 100% aW-trans retinal [73-78]. Light-adapted solubilized bacteriorhodopsin [79,80] and halorhodopsin [81-83], on the other hand, contain a mixture of about % aW-trans and /3 n-cii retinal. Dark-adaptation which takes minutes or hours, depending on conditions, results in thermally stable mixtures of /3 a -tmns and % 13-c/s chromophores in all cases. The dark-adapted 13-cis chromophores are stable because the overall shape of retinal is not very different from that of the a -trans chain, the C=N bond having assumed the syn rather than the anti configuration [84,85]. 

Cuppers, C. and E. Wagner (1950). Pharmacological effect on retinal function normal dark adaptation (German). Klin Monatsbldtter Augenheilkd 117(1) 59-69. 

Lamb, TD and Pugh, EN, 2004. Dark adaptation and the retinoid cycle of vision. Prog Retin Eye Res 23, 307-380. 

Figure 48 shows representative experimental 2H NMR spectra from the labeled retinal in bR in a dark-adapted PM sample. The line shape simulations that were generated in the data analysis are superimposed on the experimental spectra. The powder pattern [Figure 48(a)] serves as a general reference for the tilt series of spectra recorded at various sample inclinations [Figure 48(b)], because it defines the accessible frequency region over which the spectral intensity can occur. The oriented sample was measured at every 22.5° between 0° and 90°, of which three inclinations are represented in Figure 48(b) with a = 0°, 45° and 90°. 

FIGURE 48. Representative 2H NMR spectra (full lines) of dark-adapted bR (90 mg) containing deuteriated retinal, with line shape simulations (dashed lines) superimposed. Both the powder spectrum (a) from randomly oriented PM patches and the tilt series (b) over sample inclinations, a = 0, 45° and 90°, were recorded at — 60 °C (number of scans, 1.7 x 105, for a = 0°). Spectrum (c) was measured at 21 °C with a = 0° (number of scans, 3 x 105). Reprinted with permission from Reference 60. Copyright (1997) American Chemical Society... 

Fig. 2. Summary of regulatory GTPase cycle in photoactivation of cGMP-specific phosphodiesterase (PDE) in retinal rod cells. T, transducin (Gt) Rho, rhodopsin Rho, photoactivated Rho. PDE is represented as a heterotrimeric peripheral membrane protein, as is T. This regulatory cycle differs from that in Fig. 1 mainly in that the activation of PDE entails the dissociation of an inhibitory y subunit (PDEy) under the influence of activated Ta-GTP complex leading to formation of intermediary soluble Ta-GTP/PDEy complex. This complex persists until GTP is hydrolyzed to GDP, at which moment the inhibited PDEa/3y heterotrimer reforms. Dark adapted - non-activated - Rho is then required for reassociation of Ta-GDP to T/3y and release of GDP.

Figure 2. Absorption spectra of retinal isomers and rhodopsins. [Retinal spectra (in hexane at room temperature) are reproduced from refs. 52, 168, and 174.] The spectra of rhodopsin and iso-rhodopsin (A > 350 nm) are for digitonin-solubilized preparations in aqueous glycerol mixtures at 4°K (ref. 287), and room temperature (A < 350 nm. ref. 6). (Those of light-adapted (BrML) and dark-adapted (BRjjgg) bacteriorhodopsin, both for aqueous7membrane suspensions at room temperature, are reproduced from refs. 259 and 377.

Retinal pigmentary changes, visual field defects, color vision loss Retinal pigmentary changes, disturbances of dark adaptation, color vision loss, visual field defects Impairment of dark adaptation, visual field defects, vascular attenuation Color vision disturbances, entoptic phenomena Color vision disturbances... 

The peripheral lesions can occm with or without simultaneous macular involvement (Figure 35-10). Other changes include attenuated retinal vessels, optic atrophy, peripheral visual field loss, abnormal color vision, and a subnormal electroretinogram (ERG). The feet that the dark-adaptation threshold is normal, or omy minimally abnormal, further differentiates this condition flom retinitis pigmentosa. 

Thioridazine can cause significant retinal toxicity, leading to reduced visual acuity, changes in color vision, and disturbances of dark adaptation.These symptoms typically occur 30 to 90 days after initiation of treatment. The fundus often appears normal during the early stages of symptoms, but within several weeks or months a pigmentary... 

Pigmentary changes (discrete RPE pigment scattering perifoveally with depigmented surround can be in retinal periphery) accompanying CV loss, visual acuity,VF defects, decreased dark adaptation. 

The 13-c/j retinal-chromophore in dark-adapted bacteriorhodopsin exhibits a very different photocycle, whose predominant intermediate has an absorption maximum at 610 nm [199], and which contains no intermediate [202,238] analogous to M. The 610 nm intermediate will decay to either the 13-c/s chromophore or the dW-trans form, the latter pathway being responsible for the phenomenon of light-adaptation [199]. This pathway does not explain, however, why monomeric bacteriorhodopsin shows poor light-adaptation [168,239]. The chromophore in the 13-c/s configuration is not associated with proton translocation [240]. Indeed, reconstitution of bacterio-opsin with 13-demethyl retinal, which traps the retinal moiety in the 13-c/s configuration, results [241] in a non-transporting photocycle. 

In one prospective study in 17 patients with hemoljdic anemia (aged 5-25 years) lens opacities were found in 41%, changes in the retinal pigment epithelium in 35%, tortuosity of retinal vessels in 24%, dilatation and sheathing of retinal vessels in 18%, defects in color vision in 29%, and abnormal dark adaptation in 18% (56). In many other studies much lower frequencies were found. Perhaps retinal injury is related to the depletion of metals such as zinc, copper, and/or iron (57). On the other hand, ocular and auditory disturbances are not infrequent in patients with thalassemia, iron storage diseases (58,59), or uremia (45), and may be coincidental in patients receiving deferoxamine (60). 

In a study in China, electroretinographic responses and dark adaptation visual thresholds showed subtle but significant retinal dysfunction in elderly chronically transfused patients with thalassemia receiving deferoxamine (67). The authors concluded that the findings suggested that iron accumulation and not deferoxamine toxicity played a major role in these patients. 

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