Dark-adapted rods exert a tonic suppressive influence upon cone-mediated sensitivity to rapid flicker, a phenomenon called suppressive rod-cone interaction (SRC1). However, rod dark adaptation has negligible influence upon cone-mediated thresholds measured with more usual psychophysical procedures. The present study separately examined the influences of rod light and dark adaptation upon cone-mediated sensitivity to transient increases or decreases in illumination using sawtooth flicker with rapid-on (ramp-off) or rapid-off (ramp-on) waveforms. In the parafoveal retina, cones alone were stimulated with flicker by spatially superimposing longand short-wavelength stimuli presented in counterphase and matched in scotopic illuminance. Several different adaptation procedures were used. For higher (>4 Hz) frequencies, sensitivity of cones to both waveforms is nearly identical under any condition of adaptation; sensitivity decreases as rods progressively dark adapt. A considerably different situation exists for slower frequencies (1–4 Hz). Sensitivity of cones to rapid-off flicker is appreciably greater under light-adapted conditions confirming recent observations by Bowen et al. (1989). But as rods progressively dark adapt, sensitivity of cones to rapid-off waveforms decreases considerably while sensitivity to rapid-on waveforms is much less affected; in the totally dark-adapted eye, sensitivity to both waveforms is identical. These results confirm and extend recent physiological observations in amphibian retina (Frumkes & Wu, 1990) suggesting that SRCI specifically involves responses to transient decreases in illumination.

In normal observers, sensitivity of cones to rapid sinusoidal flicker decreases by about 0.7 log units as rods progressively dark adapt. However, Arden and Hogg (1985) described a night-vision disorder characterized by normal rod sensitivity but exaggerated suppressive rod-cone interaction (SRCI). We refer to this condition as the exaggerated SRCI syndrome (ESS). The present paper examines the influence of rod-adaptation upon cone-mediated responses to light onset and offset in an observer with ESS. Under all conditions of adaptation examined, sensitivity of cones to rapid-on waveforms is indistinguishable to that of a normal observer tested under identical circumstances; rod sensitivity is also normal. However, the sensitivity of cones to transient decreases in illumination is clearly subnormal under light-adapted conditions. This deficit in cone responsiveness to light offset becomes increasingly subnormal as rods dark adapt and, when completely dark adapted, the ESS observer is nearly blind to 1 Hz rapid-off sawtooth waveforms. These results strongly bolster previous results that suggest that suppressive rod-cone interaction is restricted to the response to transient decreases in illumination.

The cholinergic amacrine cells of the rabbit retina may be labeled with [3H]-Ch and the activity of the cholinergic population monitored by following the release of [3H]-ACh. We have tested the effect of muscimol, a potent GABAA agonist, on (1) the light-evoked release of ACh, presumably mediated via bipolar cells, which are known to have a direct input to the cholinergic amacrine cells and (2) ACh release produced by exogenous glutamate analogs that probably have a direct effect on cholinergic amacrine cells. Muscimol blocked the light-evoked release of ACh with an IC50 of 1.0 μM. In contrast, ACh release produced by nonsaturating doses of kainate or NMDA was not reduced even by 100 μM muscimol. Thus, we have been unable to demonstrate a direct effect of GABA on the cholinergic amacrine cells.

GABA antagonists, such as picrotoxin, caused a large increase in the base release and potentiated the light-evoked release of ACh. Both these effects were abolished by DNQX, a kainate antagonist that blocks the input to cholinergic amacine cells from bipolar cells. DNQX blocked the effects of picrotoxin even when controls showed that the mechanism of ACh release was still functional. Together, these results imply that the dominant site for the GABA-mediated inhibition of ACh release is on the bipolar cell input to the cholinergic amacrine cells. This is consistent with previous anatomical and physiological evidence that bipolar cells receive negative feedback from GABA amacrine cells.

To improve the usefulness of the ERG in identifying the sites and mechanisms of adaptation, development, and disease processes, a theoretical framework based upon Granit's analysis of the ERG was evaluated. The framework assumes that the ERG is the sum of two potentials, one, P3, generated by the receptors and the other, P2, generated by the cells of the INL. Hood and Birch (1990a, b) demonstrated that the leading edge of the a-wave can be quantitatively described by a model used to describe the response from single rod receptors. This model provides P3(t), a theoretical receptor response as a function of time, for any given flash intensity. The ERGs from normal observers and patients with retinal diseases were analyzed in this framework, first by deriving P2 by computer subtracting the predicted P3(t) responses. This analysis was successful and a computational model of the ERG was then derived. The model of P2(t) was constructed with linear filters and a static nonlinearity and using P3(t) as the input. The ERG for any given flash intensity is then P3(t) + P2(t) The model describes (1) the change both in implicit times and in trough-to-peak b–wave amplitudes with flash intensity for the normal, dark-adapted observers; and (2) the changes in b–wave implicit times and amplitudes for three patients with retinal diseases.

Among the implications drawn from these analyses were as follows: (1) The fits of the Naka-Rushton equation to trough-to-peak b–wave amplitudes must be interpreted with great care. (2) When the INL is affected by retinal disease, the b–wave may be a very poor reflection of INL activity. (3) The implicit time of the b–wave can provide a measure of receptor sensitivity.

The relation between the amplitude of visual responses to a checkerboard stimulus and the degree of lateral displacement of the checks was examined across different check sizes with simultaneously recorded electroretinograms (ERGs) and visual-evoked potentials (VEPs). The amplitudes of both the b–wave and the after-potential of the ERG increase linearly with pattern displacement. However, the major components of the VEP (N70 and P100) were smaller than expected from linearity for both small checks with small displacements (thresholding) and for large checks with large displacements (saturation). These results suggest that the ERG is proportional to the number of receptors stimulated, but the VEP reflects neural processes influenced by the spatial structure of the stimulus.

In retinas of teleost fish, neuropeptides typically have subtle, modulatory actions. The peptide effects typically have long latencies and durations, and, in some instances, they are known to be mediated by second messengers. Peptidergic neurons in teleost retinas have certain morphological features in common that are consistent with their function. Most peptidergic neurons are stratified amacrine cells with long, varicose processes; the processes of peptidergic centrifugal axons are also narrowly stratified and ramify extensively in the retina. The peptidergic amacrine cells are relatively infrequent, and, likewise, the centrifugal axons originate from a small number of perikarya in the brain. Cells that are so sparsely distributed and whose processes overlap so extensively are better-suited for modulation than for conveying detailed representations of visual space.

During the course of light adaptation, the amplitude and implicit time of the human cone ERG change systematically. In the present study, the effect of adapting field luminance on these ERG changes was assessed, and the hypothesis that light adaptation of the rod system is the primary determining factor was evaluated. Cone ERG responses, isolated through the use of 31.1-Hz flicker, were obtained from two visually normal subjects, initially under dark-adapted conditions and then repeatedly for 30 min following the onset of each of a series of ganzfeld adapting fields with luminances that ranged from –1.2 to 2.1 log cd/m. The increase in flicker ERG amplitude and decrease in implicit time during light adaptation were greatest at the highest adapting field luminances. Photopically equivalent achromatic and long-wavelength adapting fields induced comparable increases in flicker ERG amplitude, while scotopically equivalent adapting fields had considerably different effects. This latter finding demonstrates that the rod system is not a major determinant of the adaptation-induced increase in cone ERG amplitude.

Visual information is processed in a series of subsequent steps. The performance of each of these steps depends not only on the computations it performs itself but also on the representation of the visual surround on which it operates. Here we investigate the consequences of signal preprocessing for the performance of the motion-detection system of the fly. In particular, we analyze whether the retinal input signals are rectified and segregate into separate ON and OFF channels, which then feed independent parallel motion-detection pathways. We recorded the activity of an identified directionally selective interneuron (HI-cell) in response to apparent motion stimuli, i.e. sequential brightness changes at two neighboring locations in the visual field, as well as to brightness changes at only a single location. For apparent motion stimuli, the motion-dependent response component was determined by subtracting from the overall response the responses to the individual stimulus components when presented alone. The following conclusions could be derived: (1) Apparent motion consisting of a sequence of increased or decreased brightness at two locations in the visual field have the same optimum interstimulus time interval (Fig. 3). (2) Sequences of brightness steps of like polarity (either increments or decrements) elicit positive and negative motion-dependent response components when mimicking motion in the cell's preferred and null direction, respectively. The motion-dependent response components are inverted in sign when the brightness steps of a stimulus sequence have a different polarity (Fig. 7). (3) The responses to the beginning and the end of a brightness pulse depend on the pulse duration. For pulse durations of less than 2 s, both events interact with each other (Fig. 9). All of these results do not provide any indication that the fly processes motion information in independent ON and OFF motion detectors. Brightness changes of both signs are rather represented at the input of the same movement detectors, and interactions between signals resulting from both brightness increments and decrements take their sign into account. This type of preprocessing of the retinal input is argued to render a motion-detection system particularly robust against noise.

We have investigated how the binocular control of prey capture in the praying mantis is affected by abnormally large vertical disparities, which were introduced by prisms placed in front of the eyes. The position of a target on the two retinae determines both the magnitude of head saccades made to fixate a target and its perceived distance. Over the wholerange of vertical disparities tested (up to at least 30 deg), the frequency of fixating saccades is normal while the amplitude of their vertical component is a compromise between the saccades specified by each eye individually. Distance measurements are not affected by imposed vertical disparities. But the larger the vertical disparity, the more reluctant the mantid is to strike at the target until disparities exceed 15 deg when no strikes are elicited at all.

The whole-cell configuration of the patch-clamp technique was used to study voltage-gated K+ conductances in retinal ganglion cells from postnatal rat. Retinal ganglion cells were fluorescently labeled in situ, dissociated from the retina, and maintained in culture. With physiological solutions in the bath and the pipette, depolarizing voltage steps from physiological holding potentials activated Na+-(INa), Ca2+ (ICa), and K+ -currents studied previously in retinal ganglion cells. Here we report on a slowly decaying K+ current, not heretofore reported in rat. With 4-AP, TEA, and Co2+ in the bath, to block IA, IK, and IK(Ca), respectively, a slowly decaying outward current was activated from —80 mV by steps positive to —40 mV. This current was present in 92% of all ganglion cells tested (n = 83). It activated within 10 ms and inactivated with a voltage-independent time constant of about 70 ms at 35°C. Inactivation was voltage-dependent, half-maximal at —55 mV, and almost complete at 0 mV. The current was blocked by internal Cs+ and TEA, or by external application of 1 mM Ba2+, but not by 3 mM extracellular Co2+. The biophysical and pharmacological properties of this current are distinctly different from those of slowly inactivating K+ currents studied in other rat neurons. It was very similar, however, to a slowly inactivating K+ current previously reported in ganglion cells of tiger salamander retina. This last finding indicates conservation of a defined K+ channel type in functionally related cells in both lower vertebrates and mammals.