Effects Of Light Adaptation Research Articles

Visual psychophysics: Luminance and color.

Human visual psychophysics is a mature field of research that employs specialized methods and has generated a large body of established findings, a few of which are summarized in this overview. The methods reviewed include those known as classical psychophysical methods, signal detection theory, and the efficient modern Bayesian adaptive methods. The covered results emphasize well-established findings in both rod and cone vision, including some effects of light adaptation, luminous efficiency and spectral sensitivity, color detection, and spatial and temporal contrast sensitivities.

Dopamine D1 and D4 receptors contribute to light adaptation in ON-sustained retinal ganglion cells.

The adaptation of ganglion cells to increasing light levels is a crucial property of the retina. The retina must respond to light intensities that vary by 10-12 orders of magnitude, but the dynamic range of ganglion cell responses covers only ∼3 orders of magnitude. Dopamine is a crucial neuromodulator for light adaptation and activates receptors in the D1 and D2 families. Dopamine type D1 receptors (D1Rs) are expressed on horizontal cells and some bipolar, amacrine, and ganglion cells. In the D2 family, D2Rs are expressed on dopaminergic amacrine cells and D4Rs are primarily expressed on photoreceptors. However, the roles of activating these receptors to modulate the synaptic properties of the inputs to ganglion cells are not yet clear. Here, we used single-cell retinal patch-clamp recordings from the mouse retina to determine how activating D1Rs and D4Rs changed the light-evoked and spontaneous excitatory inputs to ON-sustained (ON-s) ganglion cells. We found that both D1R and D4R activation decrease the light-evoked excitatory inputs to ON-s ganglion cells, but that only the sum of the peak response decrease due to activating the two receptors was similar to the effect of light adaptation to a rod-saturating background. The largest effects on spontaneous excitatory activity of both D1R and D4R agonists was on the frequency of events, suggesting that both D1Rs and D4Rs are acting upstream of the ganglion cells.NEW & NOTEWORTHY Dopamine by bright light conditions allows retinal neurons to reduce sensitivity to adapt to bright light conditions. It is not clear how and why dopamine receptors modulate retinal ganglion cell signaling. We found that both D1 and D4 dopamine receptors in photoreceptors and inner retinal neurons contribute significantly to the reduction in sensitivity of ganglion cells with light adaptation. However, light adaptation also requires dopamine-independent mechanisms that could reflect inherent sensitivity changes in photoreceptors.

Rod and Cone Coupling Modulates Photopic ERG Responses in the Mouse Retina.

Light adaptation changes both the sensitivity and maximum amplitude (Rmax) of the mouse photopic electroretinogram (ERG) b-wave. Using the ERG, we examined how modulation of gap junctional coupling between rod and cones alters the light-adapted ERG. To measure changes, a b-wave light adaptation enhancement factor (LAEF), was defined as the ratio of Rmax after 15 min light adaptation to Rmax recorded at the onset of an adapting light. For wild-type mice (WT), the LAEF averaged 2.64 ± 0.29, however, it was significantly reduced (1.06 ± 0.04) for connexin 36 knock out (Cx36KO) mice, which lack electrical coupling between photoreceptors. Wild type mice intraocularly injected with meclofenamic acid (MFA), a gap junction blocker, also showed a significantly reduced LAEF. Degeneration of rod photoreceptors significantly alters the effects of light adaptation on the photopic ERG response. Rd10 mice at P21, with large portions of their rod photoreceptors present in the retina, exhibited a similar b-wave enhancement as wildtype controls, with a LAEF of 2.55 ± 0.19. However, by P31 with most of their rod photoreceptors degenerated, rd10 mice had a much reduced b-wave enhancement during light-adaptation (LAEF of 1.54 ± 0.12). Flicker ERG responses showed a higher temporal amplitude in mesopic conditions for WT than those of Cx36KO mice, suggesting rod-cone coupling help high-frequency signals to pass from rods to cone pathways in the retina. In conclusion, our study provides a novel method to noninvasively measure the dynamics and modulation by the light adaptation for rod-cone gap junctional coupling in intact eyes.

Inhibitory components of retinal bipolar cell receptive fields are differentially modulated by dopamine D1 receptors.

During adaptation to an increase in environmental luminance, retinal signaling adjustments are mediated by the neuromodulator dopamine. Retinal dopamine is released with light and can affect center-surround receptive fields, the coupling state between neurons, and inhibitory pathways through inhibitory receptors and neurotransmitter release. While the inhibitory receptive field surround of bipolar cells becomes narrower and weaker during light adaptation, it is unknown how dopamine affects bipolar cell surrounds. If dopamine and light have similar effects, it would suggest that dopamine could be a mechanism for light-adapted changes. We tested the hypothesis that dopamine D1 receptor activation is sufficient to elicit the magnitude of light-adapted reductions in inhibitory bipolar cell surrounds. Surrounds were measured from OFF bipolar cells in dark-adapted mouse retinas while stimulating D1 receptors, which are located on bipolar, horizontal, and inhibitory amacrine cells. The D1 agonist SKF-38393 narrowed and weakened OFF bipolar cell inhibitory receptive fields but not to the same extent as with light adaptation. However, the receptive field surround reductions differed between the glycinergic and GABAergic components of the receptive field. GABAergic inhibitory strength was reduced only at the edges of the surround, while glycinergic inhibitory strength was reduced across the whole receptive field. These results expand the role of retinal dopamine to include modulation of bipolar cell receptive field surrounds. Additionally, our results suggest that D1 receptor pathways may be a mechanism for the light-adapted weakening of glycinergic surround inputs and the furthest wide-field GABAergic inputs to bipolar cells. However, remaining differences between light-adapted and D1 receptor-activated inhibition demonstrate that non-D1 receptor mechanisms are necessary to elicit the full effect of light adaptation on inhibitory surrounds.

Dynamic Modeling of Microalgae Growth and Lipid Production under Transient Light and Nitrogen Conditions

We developed a new dynamic model to characterize how light and nitrogen regulate the cellular processes of photosynthetic microalgae leading to transient changes in the production of neutral lipids, carbohydrates, and biomass. Our model recapitulated the versatile neutral lipid synthesis pathways via (i) carbon reuse from carbohydrate metabolism under nitrogen sufficiency and (ii) fixed carbon redirection under nitrogen depletion. We also characterized the effects of light adaptation, light inhibition hysteresis, and nitrogen limitation on photosynthetic carbon fixation. The formulated model was calibrated and validated with experimental data of Dunaliella viridis cultivated in a lab-scale photobioreactor (PBR) under various light (low/moderate/high) and nitrogen (sufficient/limited) conditions. We conducted the identifiability, uncertainty, and sensitivity analyses to verify the model reliability using the profile likelihood method, the Markov chain Monte Carlo (MCMC) technique, and the extended Fourier Amplitude Sensitivity Test (eFAST). Our model predictions agreed well with experimental observations and suggested potential model improvement by incorporating a lipid degradation mechanism. The insights from our model-driven analysis helped improve the mechanistic understanding of transient algae growth and bioproducts formation under environmental variations and could be applied to optimize biofuel and biomass production.

Dopamine D1 receptor activation contributes to light-adapted changes in retinal inhibition to rod bipolar cells.

Dopamine modulation of retinal signaling has been shown to be an important part of retinal adaptation to increased background light levels, but the role of dopamine modulation of retinal inhibition is not clear. We previously showed that light adaptation causes a large reduction in inhibition to rod bipolar cells, potentially to match the decrease in excitation after rod saturation. In this study, we determined how dopamine D1 receptors in the inner retina contribute to this modulation. We found that D1 receptor activation significantly decreased the magnitude of inhibitory light responses from rod bipolar cells, whereas D1 receptor blockade during light adaptation partially prevented this decline. To determine what mechanisms were involved in the modulation of inhibitory light responses, we measured the effect of D1 receptor activation on spontaneous currents and currents evoked from electrically stimulating amacrine cell inputs to rod bipolar cells. D1 receptor activation decreased the frequency of spontaneous inhibition with no change in event amplitudes, suggesting a presynaptic change in amacrine cell activity in agreement with previous reports that rod bipolar cells lack D1 receptors. Additionally, we found that D1 receptor activation reduced the amplitude of electrically evoked responses, showing that D1 receptors can modulate amacrine cells directly. Our results suggest that D1 receptor activation can replicate a large portion but not all of the effects of light adaptation, likely by modulating release from amacrine cells onto rod bipolar cells. NEW & NOTEWORTHY We demonstrated a new aspect of dopaminergic signaling that is involved in mediating light adaptation of retinal inhibition. This D1 receptor-dependent mechanism likely acts through receptors located directly on amacrine cells, in addition to its potential role in modulating the strength of serial inhibition between amacrine cells. Our results also suggest that another D2/D4 receptor-dependent or dopamine-independent mechanism must also be involved in light adaptation of inhibition to rod bipolar cells.

The Effects of Short-Term Light Adaptation on the Human Post-Illumination Pupil Response.

We determine the effect of short-term light adaptation on the pupil light reflex and the melanopsin mediated post-illumination pupil response (PIPR). Inner and outer retinal photoreceptor contributions to the dark-adapted pupil response were estimated. In Experiment A, light adaptation was studied using short wavelength lights ranging from subthreshold to suprathreshold irradiances for melanopsin signaling that were presented before (5-60 seconds) and after (30 seconds) a melanopsin-exciting stimulus pulse. We quantified the pupil constriction and the poststimulus response amplitudes during dark (PIPR) and light (poststimulus pupil response, PSPR) adaptation. In Experiment B, colored prestimulus adapting lights were univariant for melanopsin or rod excitation. Increasing the prestimulus duration and irradiance of adapting lights increased the pupil constriction amplitude when normalized to the dark-adapted baseline but reduced its amplitude when normalized to the light-adapted baseline. Light adaptation at irradiances suprathreshold for melanopsin activation increased the PIPR amplitude, with larger changes at longer adaptation durations, whereas the PSPR amplitude became more attenuated with increasing irradiances, independent of duration. Rod versus melanospin univariant adaptation did not alter the constriction amplitude but increased the PIPR amplitude in the rod condition. Correlations between millimeter pupil constriction and PIPR amplitudes were eliminated when normalized to the baseline diameter. The findings have implications for standardizing light adaptation paradigms and the choice of pupil metrics in both laboratory and clinical settings. Light and dark adaptation have opposite effects on the pupil metrics, which should be normalized to baseline to minimize significant correlations between constriction and PIPR amplitudes.

Effects of imagery-induced light adaptation on the detection of luminance increments and decrements

Effects of imagery-induced light adaptation on the detection of luminance increments and decrements

Light increases the gap junctional coupling of retinal ganglion cells

We examined the effect of light adaptation on the gap junctional coupling of α-ganglion cells (α-GCs) in rabbit and mouse retinas. We assayed changes in coupling by measuring parameters of tracer coupling following injection of α-GCs with Neurobiotin and the concerted spike activity of α-GC neighbours under dark- and light-adapted conditions. We found that light adaptation using mesopic or photopic background lights resulted in a dramatic increase in the labelling intensity, number, and spatial extent of ganglion and amacrine cells coupled to OFF α-GCs when compared to levels seen under dark adaptation. While this augmentation of coupling by light did not produce an increase in the concerted spontaneous activity of OFF α-GC neighbours, it did significantly increase correlated light-evoked spiking. This was seen as an increase in the number of correlated spikes for α-GC neighbours and an extension of correlations to second-tier neighbours that was not seen under dark-adapted conditions. Pharmacological studies in the rabbit retina indicated that dopamine mediates the observed changes in coupling by differentially activating D1 and D2 receptors under different adaptation states. In this scheme, activation of dopamine D1 receptors following light exposure triggers cAMP-mediated intracellular pathways resulting in an increase in gap junctional conductance. Overall, our results indicate that as we move from night to day there is an enhanced electrical coupling between α-GCs, thereby increasing the concerted activity believed to strengthen the capacity and efficiency of information flow across the optic nerve.

Asymmetrical growth of the photopic hill during the light adaptation effect

In response to progressively stronger flashes delivered against a rod saturating background light, the amplitude of the photopic ERG b-wave first increases, reaches a maximal value (V (max)) and then decreases gradually to a plateau where the amplitude of the b-wave equals that of the a-wave, a phenomenon known as the photopic hill (PH). The purpose of this study was to investigate how the PH grew during the course of the light adaptation (LA) process that follows a period of dark adaptation (DA): the so-called light adaptation effect (LAE). Photopic ERG (time-integrated) luminance-response (LR) functions were obtained prior to (control-fully light adapted) and at 0, 5 and 10min of LA following a 30-min period of DA. A mathematical model combining a Gaussian and a logistic growth function, suggested to reflect the OFF and ON retinal contribution to the PH respectively, was fitted to the LR functions thus obtained. Our results indicate that the magnitude of the cone ERG LAE is modulated by the stimulus luminance, with b-wave enhancements being maximal for luminance levels that result in the descent of the PH. The Gaussian function grew significantly with LA while the logistic growth function remained basically unchanged. Our findings would therefore suggest that the LAE reflects primarily an increase in the retinal OFF response during LA.

Human scotopic sensitivity is regulated postreceptorally by changing the speed of the scotopic response

Sensitivity regulation enables the visual system to function effectively from the absorption of a few photons at the lowest visual threshold to the absorption of enough photons to bleach nearly all the light-sensitive photopigment in the eye. Here, we investigate sensitivity regulation in the rod (or scotopic) range from -3.8 to -0.8 log(10) scotopic trolands. Over most of this range, the rate of photon absorption per rod is too low for sensitivity regulation to be practicable within the rod photoreceptor itself, so that regulation must occur postreceptorally. We measured adaptation-dependent changes in visual sensitivity and visual delay, which together provide a much more complete characterization of the effects of light adaptation than the usual method of measuring sensitivity changes alone. Our results demonstrate clearly that changes in scotopic sensitivity with increasing light levels are achieved in large part by a speeding up of the scotopic response and a decrease in the temporal integration time. Thus, the scotopic and the photopic systems both regulate their steady-state sensitivity using the same strategy, even though the scotopic system does it largely postreceptorally and the photopic system largely receptorally.

Toward clinical application of manganese-enhanced MRI of retinal function

Purpose The application of manganese-enhanced MRI (MEMRI) to measure retinal function in humans is unclear. To begin to address this gap, we tested the hypothesis that an FDA-approved manganese-based MRI contrast agent, Teslascan, is useful for measuring functional intraretinal ionic regulation. Methods Anesthetized dark- or light-adapted male healthy Sprague–Dawley rats were infused for 30 min with 10 μmol/kg of Teslascan (clinically relevant dose; n = 5), 100 μmol/kg Teslascan ( n = 5), or saline ( n = 5). Four hours post-administration, high resolution MEMRI data were collected. Intraretinal signal intensities and enhancements were measured. Modelling was performed to estimate apparent retinal transfer constant K i and to determine optimal data acquisition parameters. Results In light-adapted rats, intraretinal enhancements responded in a dose–response manner. In addition, in the outer retina the effect of light-adaptation was to reduce significantly Mn 2+ uptake and K i compared to dark-adaptation. A non-significant change was also observed in the inner retina. Modelling shows Mn 2+ plasma concentration reaching a plateau after about 2 h. Apparent K i values for the clinically relevant dose are 3–6 × 10 −3 min −1, decreasing to 0.5–0.6 × 10 −3 min −1 at the higher dose. Intraretinal signal is almost linear with K i . Optimal TR for a spin-echo sequence is 0.4–1.4 s. Conclusion First time evidence is presented that a clinically relevant dose and route of Teslascan can be used to measure intraretinal function. The potential for future clinical application of MEMRI in a broad range of retinopathies is high.

Connexin57 is expressed in dendro‐dendritic and axo‐axonal gap junctions of mouse horizontal cells and its distribution is modulated by light

Mouse horizontal cells are coupled by gap junctions composed of connexin57. These gap junctions are regulated by ambient light via multiple neuromodulators including dopamine. In order to analyze the distribution and structure of horizontal cell gap junctions in the mouse retina, and examine the effects of light adaptation on gap junction density, we developed antibodies that detect mouse retinal connexin57. Using immunohistochemistry in retinal slices, flat-mounted retinas, and dissociated retinal cells, we showed that connexin57 is expressed in the dendrites and axon terminal processes of mouse horizontal cells. No staining was found in retinas of connexin57-deficient mice. Significantly more connexin57-positive puncta were found in the distal than in the proximal outer plexiform layer, indicating a higher level of expression in axon terminal processes than in the dendrites. We also examined the gap junctions using immunoelectron microscopy and showed that connexin57 does not form hemichannels in the horizontal cell dendritic tips. Light adaptation resulted in a significant increase in the number of connexin57-immunoreactive plaques in the outer plexiform layer, consistent with previously reported effects of light adaptation on connexin57 expression in the mouse retina. This study shows for the first time the detailed location of connexin57 expression within mouse horizontal cells, and provides the first ultrastructural data on mouse horizontal cell gap junctions.

Kinetics of Turn-offs of Frog Rod Phototransduction Cascade

The time course of the light-induced activity of phototrandsuction effector enzyme cGMP-phosphodiesterase (PDE) is shaped by kinetics of rhodopsin and transducin shut-offs. The two processes are among the key factors that set the speed and sensitivity of the photoresponse and whose regulation contributes to light adaptation. The aim of this study was to determine time courses of flash-induced PDE activity in frog rods that were dark adapted or subjected to nonsaturating steady background illumination. PDE activity was computed from the responses recorded from solitary rods with the suction pipette technique in Ca2+-clamping solution.A flash applied in the dark-adapted state elicits a wave of PDE activity whose rising and decaying phases have characteristic times near 0.5 and 2 seconds, respectively. Nonsaturating steady background shortens both phases roughly to the same extent. The acceleration may exceed fivefold at the backgrounds that suppress ≈70% of the dark current.The time constant of the process that controls the recovery from super-saturating flashes (so-called dominant time constant) is adaptation independent and, hence, cannot be attributed to either of the processes that shape the main part of the PDE wave. We hypothesize that the dominant time constant in frog rods characterizes arrestin binding to rhodopsin partially inactivated by phosphorylation. A mathematical model of the cascade that considers two-stage rhodopsin quenching and transducin inactivation can mimic experimental PDE activity quite well. The effect of light adaptation on the PDE kinetics can be reproduced in the model by concomitant acceleration on both rhodopsin phosphorylation and transducin turn-off, but not by accelerated arrestin binding. This suggests that not only rhodopsin but also transducin shut-off is under adaptation control.

Functional Mechanisms Shaping Lateral Geniculate Responses to Artificial and Natural Stimuli

Functional models of the early visual system should predict responses not only to simple artificial stimuli but also to sequences of complex natural scenes. An ideal testbed for such models is the lateral geniculate nucleus (LGN). Mechanisms shaping LGN responses include the linear receptive field and two fast adaptation processes, sensitive to luminance and contrast. We propose a compact functional model for these mechanisms that operates on sequences of arbitrary images. With the same parameters that fit the firing rate responses to simple stimuli, it predicts the bulk of the firing rate responses to complex stimuli, including natural scenes. Further improvements could result by adding a spiking mechanism, possibly one capable of bursts, but not by adding mechanisms of slow adaptation. We conclude that up to the LGN the responses to natural scenes can be largely explained through insights gained with simple artificial stimuli.

Photosynthetic responses to Cu 2+ exposure are independent of light acclimation and uncoupled from growth inhibition in Fucus serratus (Phaeophyceae)

We have studied the effect of light acclimation on photosynthetic responses and growth during Cu 2+ exposure (0–0.84 μM) in the brown seaweed Fucus serratus. Measurements of chlorophyll fluorescence parameters showed that Cu 2+ exposure amplified ETR, reduced the chlorophyll content at the cellular level and that there was no effect of light adaptation on the Cu 2+ resistance of the algae. In contrast to the inhibitory effects of Cu 2+ on chlorophyll fluorescence, O 2 evolution and the total content of chlorophyll and carotenoid of the algae was unaffected by Cu 2+. We conclude that photoinhibition and perhaps pigment degradation in the meristoderm was compensated for by cells deeper in the thallus with the result that the overall photosynthetic fitness of the algae was maintained. The pronounced inhibitory effects of Cu 2+ on algae growth was not a consequence of photoinhibition and could be attributed to direct inhibitory effects on the growth process.

Effects of light and dark adaptation of rods on specific-hue threshold

Specific-hue threshold as a function of absolute rod threshold was measured with long-, middle-, and short-wavelength monochromatic test lights presented 17 deg extrafoveally. The measurements were obtained both during the rod phase of long-term dark adaptation and under conditions where the rod receptor system was gradually light adapted from a dark-adapted state by a scotopic background field of increasing retinal illumination. The results show that change in specific-hue threshold with change in absolute rod threshold is not, in general, identical for light and dark adaptation of the rod receptor system. Thus, in the long- and middle-wavelength test regions, the specific-hue threshold could be obtained at higher intensities under the light- as compared to the dark-adaptation condition when absolute rod thresholds were the same. Just the opposite was found for the short-wavelength tests. It is concluded that change in specific-hue threshold with light and dark adaptation of the rod receptor system is not, in general, controlled by the same mechanism.

Effects of Light Adaptation on the Temporal Resolution of Deep-sea Crustaceans

The effects of light adaptation on flicker fusion frequency were examined in the photoreceptors of 13 species of deep-sea crustaceans. Light adaptation produced a significant increase in the maximum critical flicker fusion frequency (CFF(max)) in 7 species-all 6 species of euphausiids in the study, and 1 species of oplophorid (Group 1). This is the first example of an increase in temporal resolution due to light adaptation in a deep-sea species. In the other six species-2 oplophorids, 1 pandalid, 1 pasiphaeid, 1 penaeid and 1 sergestid (Group 2)-light adaptation had no effect, or resulted in a decrease in the flicker fusion frequency. The mean dark-adapted CFF(max) of the Group 1 species was significantly higher, and the mean response latency significantly lower, than those of the Group 2 species. Possible explanations for these differences include the activity and bioluminescence mode of preferred prey items, as well as the retention of larval/juvenile adaptations in adult eyes.

Effect of light and oxygen and adaptation to changing light conditions in a photosynthetic mutant in which the LHII complex of Rhv. sulfidophilum was heterologously expressed in a strain of Rb. capsulatus whose puc operon was deleted.

In this paper we show the effect of oxygen and light on the expression of the photosynthetic apparatus of a mutant heterologously expressing the puc operon. This mutant was obtained by introducing in trans an expression plasmid, bearing the puc A, B, and C genes of Rhv. sulfidophilum, as well as its own promoter, in an LHII(-) mutant of Rb. capsulatus. The results showed that oxygen and light repressed LHII expression. Even low-light intensities lowered the LHII content to undetectable levels by spectrophotometry or by SDS-PAGE. In high-light grown cells, where the relative ratios of LHI and LHII complexes were significantly diminished, we were able to detect LHII complexes. Under the latter condition, the absorption spectrum showed that some pigment accumulated in the membrane even in the absence of cell division. These pigments were used in a later step to assemble LHII complexes, when the high-light grown cells were transferred to semiaerobiosis in the dark. Transition of high-light grown cells to low-light conditions allowed us to study the adaptability of these heterologous mutant cells. We observed that adaptation never occurred, in part probably owing to energy limitation.

Effects of light adaptation on contrast processing in bipolar cells in the retina.

Effects of light adaptation on contrast processing in the outer retina were investigated over nearly four decades of background illumination by analyzing the intracellular responses of 111 bipolar cells, 66 horizontal cells, and 22 cone photoreceptors in the superfused eyecup of the tiger salamander (Ambystoma tigrinum). Light adaptation had striking and similar effects on the average contrast responses of the hyperpolarizing (Bh) and depolarizing (Bd) classes of bipolar cells: Over the lower two decades of background illumination, the contrast gain increased 7-fold to reach values as high as 20-30, the dynamic range and the half-maximum contrast decreased by about 60%, the total voltage range increased some 40%, and contrast dominance changed from highly positive to more balanced. At higher levels of background, most aspects of the contrast response stabilized and Weber's Law then held closely. In this background range, the contrast gain of bipolar cells was amplified some 20X relative to that of cones whereas the corresponding amplification in horizontal cells was about 6X. Differences in the growth of contrast gain with the intensity of the background illumination for cones versus bipolar cells suggest that there are at least two adaptation-dependent mechanisms regulating contrast gain. One is evident in the cone photoresponse such that an approximately linear relation holds between the steady-state hyperpolarization and contrast gain. The other arises between the voltage responses of the cones and bipolar cells. It could be presynaptic (modulation of cone transmitter release by horizontal cell feedback or other mechanisms) and/or postsynaptic, that is, intrinsic to bipolar cells. Contrast gain grew with the background intensity by a larger factor in horizontal than in bipolar cells. This provides a basis for the widely held view that light adaptation increases the strength of surround antagonism in bipolar cells. On average, the effects of light adaptation and most quantitative indices of contrast processing were remarkably similar for Bd and Bh cells, implying that both classes of bipolar cells, despite possible differences in underlying mechanisms, are about equally capable of encoding all primary aspects of contrast at all levels of light adaptation.