Calretinin-containing retinal amacrine cells are heterogeneous with regard to their neurochemical properties. In the rabbit retina, about 90% of them contain glycine, as evidenced in the present study by double-label immunocytochemistry. In a previous report, we showed that a small population of amacrine cells contains both γ-aminobutyric acid and calretinin. In this study, we further identified this cell population by means of known secondary markers. However, none of the markers we tested (choline acetyltransferase, serotonin accumulation, NADPH-diaphorase, vasoactive intestinal polypeptide) co-localized with calretinin. A small population (1%) of the cells in the ganglion cell layer contains both calretinin and glycine. Since calretinin-positive cells in the ganglion cell layer have been identified as ganglion cells based on soma size and presence of calretinin-positive axons in the optic nerve fiber layer, this population may represent a class of ganglion cell which contains glycine. Our results, together with those of other studies, suggest that calretinin is not a general marker of any of the well-known amacrine cell types in the mammalian retina. Rather, calretinin, just as other calcium-binding proteins, is distributed in a species-specific manner. At the same time it appears that, as shown for horizontal cells, one or more of the major buffer-type calcium-binding proteins of the EF-hand family is present in most of the retinal amacrine cells.

A nonlinear interaction between signals from at least two spatially displaced receptors is a fundamental requirement for a direction-selective motion detector. This paper characterizes the nonlinear mechanism present in the motion detector pathway that provides the input to wide-field directional neurons in the nucleus of the optic tract of the wallaby, Macropus eugenii. An apparent motion stimulus is used to reveal the interactions that occur between adjacent regions of the receptive fields of the neurons. The interaction between neighboring areas of the field is a nonlinear facilitation that is accurately predicted by the outputs of an array of correlation-based motion detectors (Reichardt detectors). Based on the similarity between the output properties of the detector array and the real neurons, it is proposed that the interaction between neighboring regions of the receptive field is a second-order nonlinearity such as a multiplication. The results presented here for wallaby neurons are compared to data collected from directional systems in other species.

In the visual system, nearby neurons of similar functional type have a tendency to fire synchronously. Cross-correlation analysis of spike discharges recorded from pairs of neurons has revealed that the synchronized activity is frequently associated with oscillatory firing patterns. However, the underlying neural mechanisms and functions of synchronization and oscillations are not well understood. In the present study, we simultaneously recorded spike discharges from multiple OFF-sustained type ganglion cells with no antagonistic surround (the dimming detectors) of the frog retina using a planar multi-electrode array and analyzed the temporal properties of light-evoked spike discharges. With full-field, temporally modulated diffuse illumination, cross-correlation analysis revealed the presence of the synchronous oscillatory pattern. The strength of the synchronized activity decreased slightly with increased intercellular distance. Synchronized spike discharges were detected even in cell pairs more than 2 mm apart. The frequency of oscillations peaked at approximately 30 Hz. The shuffled cross-correlogram was nearly flat, indicating that the synchronous oscillatory activities are most probably of neural origin. When GABAA antagonists were applied to the retina, oscillations were suppressed almost completely and the strength of the synchronized activity decreased with increased intercellular distance more sharply than control. When small spot illumination was applied to the overlapping receptive fields of an adjacent cell pair, a weak synchronized activity was evoked without accompanying oscillations. The same cell pair generated a strong synchronized activity accompanied with oscillations with full-field illumination. Our results suggest that local synchronous activities are generated via short-range neural interactions, and that the oscillatory activities are induced by long-range neural interactions and may contribute to the establishment of synchrony between widely separated neuronal populations.

Based on previous evidence that acetylcholine (ACh) and noradrenaline (NA) play a permissive role in developmental plasticity in the kitten visual cortex, we reinvestigated this topic in the postnatal visual cortex of rats with normal vision. In rats, the functional properties of visual cortical cells develop gradually between the second and the sixth postnatal week (Fagiolini et al., 1994). Cortical cholinergic depletion, by basal forebrain (BF) lesions at postnatal day (PD) 15 (eye opening), leads to a transient disturbance in the distribution of ocular dominance (Siciliano et al., 1997). In the present study, we investigated the development of visual cortical response properties following cytotoxic lesions of the locus coeruleus (LC) alone or in combination with lesions of cholinergic BF. The main result is that early NA depletion impairs the orientation selectivity of cortical neurons, causes a slight increase of their receptive-field size, and reduces the signal-to-noise ratio of cell responses. Similar effects are obtained following NA depletion in adult animals, although the effects of adult noradrenergic deafferentation are significantly more severe than those obtained after early NA depletion. Additional cholinergic depletion causes an additional transient change in ocular-dominance distribution similarly to that obtained after cholinergic deafferentation alone. Comparisons between depletion of NA on the one hand and depletion of both NA and ACh on the other suggest that the effects of combined deafferentation on the functional properties studied result from simple linear addition of the effects of depleting each afferent system alone.

In mammals, gap junctions between retinal bipolar cells are generally small and tracer coupling has not been previously demonstrated. In this study, Neurobiotin was injected into the Ba3-type cone bipolar cell, a medium-field cone bipolar cell that ramifies in sublamina a of the rabbit retina. Tracer spread to many other Ba3 bipolar cells, presumably through gap junctions. It also spread to a smaller field bipolar cell called the Ba1 that ramifies at the same depth of the inner plexiform layer. Injection of Neurobiotin into Ba1 bipolar cells did not produce staining beyond the injected cell. Tracer coupling from the Ba3 was therefore both heterologous, in that different cell types were stained, and asymmetric. The unusual properties of this bipolar cell suggest that its function may differ from that of most cone bipolar cells, which are narrow-field, do not overlap, and are poorly coupled to one another.

The hamster intergeniculate leaflet (IGL), part of the circadian rhythm regulatory system, has very extensive interconnections with subcortical visual nuclei. The present investigation describes IGL connections with the hamster diencephalon and telencephalon and compares them with ventral lateral geniculate nucleus (VLG) connections and retinal projections. Connections of the geniculate nuclei were evaluated using anterograde transport of iontophoretically injected Phaseolus vulgaris leucoagglutinin and by retrograde transport of cholera toxin β fragment. The cholera fragment was also injected intraocularly to trace retinal efferents. The IGL has ipsilateral and contralateral projections to the anterior and posterior hypothalamic nuclei, the ventral preoptic, lateral and dorsal hypothalamic areas, but not to the core ventromedial nucleus and very sparsely to the paraventricular nucleus. There are also IGL projections to the medial and lateral zona incerta, anteroventral, anterodorsal, reuniens, parataenial, paraventricular, centrolateral, central medial, and laterodorsal thalamic nuclei. IGL projections to the telencephalon are found in the horizontal limb of the diagonal band, olfactory tubercle, nucleus of the lateral olfactory tract, posterior bed nucleus of the stria terminalis, ventral pallidum, and in nuclei of the medial amygdala. The only substantial VLG projections are to bed nucleus of the stria terminalis, IGL, medial zona incerta, central medial and laterodorsal thalamic nuclei. Several of the IGL targets, the bed nucleus of the stria terminalis and zona incerta in particular, send projections back to the IGL and VLG. In addition, cells are present in the caudal cingulate cortex that project to both nuclei. Retinal projections are found in many of the regions receiving IGL innervation, including nuclei of the medial basal telencephalon, the posteromedial bed nucleus of the stria terminalis, and nuclei of the hypothalamus. A retinal projection is also visible in the lateral olfactory tract from which it extends rostrally, then medially along the base of the rhinal fissure. Fibers also extend caudally, in a superficial location, to perirhinal cortex. The results further demonstrate the widespread connections of the IGL and support the idea that the IGL modulates olfactory, photic, and circadian rhythm regulation of regulatory physiology and behavior.

The position, size, and shape of the receptive field (RF) of some cortical neurons change dynamically, in response to artificial scotoma conditioning (Pettet & Gilbert, 1992) and to retinal lesions (Chino et al., 1992; Darian-Smith & Gilbert, 1995) in adult animals. The RF dynamics are of interest because they show how visual systems may adaptively overcome damage (from lesions, scotomas, or other failures), may enhance processing efficiency by altering RF coverage in response to visual demand, and may perform perceptual learning. This paper presents an afferent excitatory synaptic plasticity rule and a lateral inhibitory synaptic plasticity rule—the EXIN rules (Marshall, 1995)—to model persistent RF changes after artificial scotoma conditioning and retinal lesions. The EXIN model is compared to the LISSOM model (Sirosh et al., 1996) and to a neuronal adaptation model (Xing & Gerstein, 1994). The rules within each model are isolated and are analyzed independently, to elucidate their roles in adult cortical RF dynamics. Based on computer simulations, the EXIN lateral inhibitory synaptic plasticity rule and the LISSOM lateral excitatory synaptic plasticity rule produced the best fit with current neurophysiological data on visual cortical plasticity in adult animals (Chino et al., 1992; Pettet & Gilbert, 1992; Darian-Smith & Gilbert, 1995) including (1) the retinal position and shape of the expanding RFs; (2) the corticotopic direction in which responsiveness returns to the silenced cortex; (3) the direction of RF shifts; (4) the amount of change in response to blank stimuli; and (5) the lack of dynamic RF changes during conditioning with a retinal lesion in one eye and the unlesioned eye kept open, in adult animals. The effects of the LISSOM lateral inhibitory synaptic plasticity rule during artificial scotoma conditioning are in conflict with those of the other two LISSOM synaptic plasticity rules. A novel “complementary scotoma” conditioning experiment, in which stimulation of two complementary regions of visual space alternates repeatedly, is proposed to differentiate the predictions of the EXIN and LISSOM rules.

Extensive evidence has suggested a trophic role of γ-aminobutyric acid (GABA) on developing cone photoreceptors in postnatal retina. In a previous study, we showed that GABA raises intracellular calcium levels in the developing cones via activation of GABAA receptors. Using confocal microscopy in conjunction with immunocytochemistry, we have now demonstrated that (1) GABAA receptor subunits are localized on cone cell bodies as well as on cone pedicles, indicating that GABA has a direct, rather than indirect, effect on cones and (2) the temporal expression of GABAA receptor subunits coincides with the developmental effects of GABA on cone synaptogenesis. An antibody against the β 2/3 subunits of the GABAA receptor and a specific cone marker peanut-agglutinin lectin (PNA) were used to double-label wholemount neonatal retinal preparations. Results show that GABAA receptors are transiently expressed on cone photoreceptors in the early stages of postnatal retinal development. GABAA receptor immunoreactivity is clearly present on cone cell bodies and their processes and on other—as yet unidentified—elements (horizontal cells?) in the outer plexiform layer. Immunoreactivity decreases within cone photoreceptor somata after postnatal day 5, but persists in the processes of the outer plexiform layer until day 7. Our results provide support for the hypothesis that GABA acts as an important developmental regulator of cone photoreceptor maturation.

Our objective with this study was to provide a near complete characterization of how mean light level changes the spatial receptive-field properties of X-cells. Single X-cells were recorded extracellularly either from cell bodies in the retina or from their axons in the optic tract. Frequency responses of the cells at 2 Hz were measured for a set of gratings of different spatial frequencies and for a stimulus designed to probe the spatial properties of the receptive-field surround. Predicted frequency responses of a Gaussian center-surround model for the receptive field were fit simultaneously to both sets of measurements and the parameters of the model that best fit the data used to characterize the spatial properties of the receptive field. Measurements were made at a number of mean light levels for each cell and changes in receptive-field properties were characterized by changes in the parameters of the Gaussian center-surround model. The range of illuminances studied covered the bulk of the range encountered by a cat naturally and three distinct functional ranges appeared to express themselves in the data. One range corresponded to the cat's photopic range of vision. The other two ranges were where signals originating in rods dominate X-cell responses. We argue that one corresponds to the range that rod signals pass predominantly through rod bipolars en route to the X-cell, while the other is where rod signals flow predominantly through cones via gap junctions and then follow the path of cone signals to the X-cell. Among the major findings are that Weber's Law is followed throughout the photopic but not the scotopic range, that center radius expands under scotopic conditions, and that the surround is present even at the lowest scotopic levels we studied.

AMPA-selective glutamate receptors play a major role in glutamatergic neurotransmission in the retina and are expressed in a variety of neuronal subpopulations. In the present study, immunocytochemical techniques were used to visualize the distribution of GluR2 and GluR4 subunits in the cat retina. Results were compared with previous localizations of GluR1 and GluR2/3. Staining for GluR2 was limited to a small number of amacrine and ganglion cells whereas GluR4 staining was present in A-type horizontal cells, many amacrine cells including type AII amacrine cells, and the majority of the cells in the ganglion cell layer. Analysis of synaptic relationships in the outer plexiform layer showed the GluR4 subunit to be concentrated at the contacts of cone photoreceptors with A-horizontal cells. In the inner plexiform layer, both GluR2 and GluR4 were postsynaptic to cone bipolar cells at dyad contacts although GluR2 staining was limited to one of the postsynaptic elements whereas GluR4 immunoreactivity was often seen in both postsynaptic elements. Unlike GluR2, GluR4 was also postsynaptic to rod bipolar cells where it could be visualized in processes of AII amacrine cells. The data indicate that GluR3 and GluR4 subunits are colocalized in a number of cell types including A-type horizontal cells, AII amacrine cells, and alpha ganglion cells, but whether they are combined in the same multimeric receptors remains to be determined.

Orientation selectivity is one of the most conspicuous receptive-field (RF) properties that distinguishes neurons in the striate cortex from those in the lateral geniculate nucleus (LGN). It has been suggested that orientation selectivity arises from an elongated array of feedforward LGN inputs (Hubel & Wiesel, 1962). Others have argued that cortical mechanisms underlie orientation selectivity (e.g. Sillito, 1975; Somers et al., 1995). However, isolation of each mechanism is experimentally difficult and no single study has analyzed both processes simultaneously to address their relative roles. An alternative approach, which we have employed in this study, is to examine the relative contributions of linear and nonlinear mechanisms in sharpening orientation tuning. Since the input stage of simple cells is remarkably linear, the nonlinear contribution can be attributed solely to cortical factors. Therefore, if the nonlinear component is substantial compared to the linear contribution, it can be concluded that cortical factors play a prominent role in sharpening orientation tuning. To obtain the linear contribution, we first measure RF profiles of simple cells in the cat's striate cortex using a binary m-sequence noise stimulus. Then, based on linear spatial summation of the RF profile, we obtain a predicted orientation-tuning curve, which represents the linear contribution. The nonlinear contribution is estimated as the difference between the predicted tuning curve and that measured with drifting sinusoidal gratings. We find that measured tuning curves are generally more sharply tuned for orientation than predicted curves, which indicates that the linear mechanism is not enough to account for the sharpness of orientation-tuning. Therefore, cortical factors must play an important role in sharpening orientation tuning of simple cells. We also examine the relationship of RF shape (subregion aspect ratio) and size (subregion length and width) to orientation-tuning halfwidth. As expected, predicted tuning halfwidths are found to depend strongly on both subregion length and subregion aspect ratio. However, we find that measured tuning halfwidths show only a weak correlation with subregion aspect ratio, and no significant correlation with RF length and width. These results suggest that cortical mechanisms not only serve to sharpen orientation tuning, but also serve to make orientation tuning less dependent on the size and shape of the RF. This ensures that orientation is represented equally well regardless of RF size and shape.

Vernier onset/offset thresholds were measured both psychophysically and with the steady-state VEP by introducing a series of horizontal breaks in a vertical square-wave luminance grating. Several diagnostic tests indicated that the first harmonic component of the evoked response generated by periodic modulation of offset gratings taps mechanisms that encode the relative position of spatial features. In the first test, a first harmonic component was only found with targets that contained transitions between collinear and noncollinear states. VEP vernier onset/offset thresholds obtained with foveal viewing were in the range of 15–22 arc sec. Control experiments with transitions between symmetrical, noncollinear patterns (relative motion) did not produce first harmonic components, nor did full-field motion of a collinear grating. A second series of experiments showed that VEP thresholds based on the first harmonic component of the vernier onset/offset response had an eccentricity dependence that was very similar to that found in a psychophysical discrimination task that required a left/right position judgment (vernier acuity). Other recordings showed that the first harmonic of the vernier onset/offset VEP was degraded by the introduction of a gap between stimulus elements, as is the displacement threshold. The vernier onset/offset target also produced a second harmonic component that was virtually identical to the one produced by a relative motion stimulus. Displacement thresholds based on these second harmonic components showed a more gradual decline with retinal eccentricity than did the first harmonic component elicited by vernier offsets. The second harmonic of the vernier onset/offset VEP was relatively unaffected by the introduction of gaps between the stimulus elements. The first and second harmonic components of the vernier onset/offset VEP thus tap different mechanisms, both of which support displacement thresholds that are finer than the resolution limits set by the spacing of the photoreceptors (hyperacuity).

Bipolar cells are not only important for visual processing but input from these cells may underlie the reorganization of ganglion cell dendrites in the inner plexiform layer (IPL) during development. Because little is known about the development of bipolar cells, here we have used immunocytochemical markers and dye labeling to identify and follow their differentiation in the neonatal ferret retina. Putative cone bipolar cells were immunoreacted for calbindin and recoverin, and rod bipolar cells were immunostained for protein kinase C (PKC). Our results show that calbindin-immunoreactive cone bipolar cells appear at postnatal day 15 (P15), at which time their axonal terminals are already localized to the inner half of the IPL. By contrast, recoverin-immunoreactive cells with terminals in the IPL are present at birth, but many of these cells may be immature photoreceptors. By the second postnatal week, recoverin-positive cells resembling cone bipolar cells were clearly present, and with increasing age, two distinct strata of immunolabeled processes occupied the IPL. PKC-containing rod bipolar cells emerged by the fourth postnatal week and at this age have stratified arbors in the inner IPL. The early bias of bipolar axonal arbors in terminating in the inner or outer half of the IPL is confirmed by dye labeling of cells with somata in the inner nuclear layer. At P10, several days before ribbon synapses have been previously observed in the ferret IPL, the axon terminals of all dye-labeled bipolar cells were clearly stratified. The results suggest that bipolar cells could provide spatially localized interactions that are suitable for guiding dendritic lamination in the inner retina.

We have characterized a distinctive type of bistratified amacrine cell in the rabbit retina at both the single cell and population levels. These cells correspond to the “fountain” amacrine cells recently identified by MacNeil and Masland (1998). The fountain cells can be distinguished in superfused retinal wholemounts labeled with nuclear dyes, thus enabling them to be targeted for intracellular injection with Neurobiotin. This revealed that the primary dendrites ascend steeply to sublamina b of the inner plexiform layer, where they form an irregular arbor at the border of strata 4 and 5. These dendrites then give rise to multiple varicose processes that descend obliquely to sublamina a, where they form a more extensive arbor in stratum 1. The fountain amacrine cells show strong homologous tracer coupling when injected with Neurobiotin, and this has enabled us to map their density distribution across the retina and to examine the dendritic relationships between neighboring cells. The fountain amacrine cells range in density from 90 to 360 cells/mm2 and they account for 1.5% of the amacrine cells in the rabbit retina. The thick tapering dendrites in sublamina b form highly territorial arbors that tile the retina with minimal overlap, whereas the thin varicose processes intermingle in sublamina a. The fountain cells are immunopositive for γ-aminobutyric acid and immunonegative for glycine. We further propose that these cells are homologous to the substance P-immunoreactive (SP-IR) amacrine cells in the cat retina and that they may account for a subset of the SP-IR amacrine cells in the rabbit retina.

To better understand the mechanisms of extracellular space volume regulation and their possible effects on retinal function, light-induced changes in the concentrations of the principal extracellular ions (Na+, K+, Ca2+, and Cl−) were measured with ion-sensitive microelectrodes in the chick retina–pigment epithelium–choroid preparation. Changes of extracellular space volume were assessed by measuring the concentration of an impermeant marker, tetramethylammonium. In the inner retina, transient ON/OFF Na+ decrease was about twice as large as K+ increase, and the charge difference was compensated by a decrease in Cl− concentration. The ion changes were accompanied by extracellular space-volume decreases here. In the subretinal space, [Na+]o increase was about twice as large as K+ decrease, yet [Cl−]o also decreased; this was accompanied by a sustained extracellular space-volume increase. The ionic changes in the inner retina are consistent with a model of extracellular space-volume regulation which assumes that neuronal depolarization causes net uptake of NaCl, cell swelling, and extracellular space shrinkage. However, to prevent the apparent violation of electroneutrality in the subretinal space, our simple model should be expanded to include the involvement of unidentified anion(s). Substantial changes in the subretinal space volume may influence interaction between the neural retina and pigment epithelium. Among ionic changes, only the light-induced [K+]o decrease around the photoreceptors and the [Ca2+]o increase near the photoreceptor bodies and synaptic terminals are large enough (−25% and 7.5%, respectively) to be likely candidates for integrated intercellular signaling.

Glutamate and γ-aminobutyric acid (GABA) are the dominant amino acids in the retina and brain. The manufacturing and degradation pathways of both of these amino acids are intricately linked with the tricarboxylic acid cycle leading to rapid redistribution of these amino acids after metabolic insult. Postmortem ischemia in mammalian retina predominantly results in a loss of glutamate and GABA from neurons and accumulation of these amino acids within Müller cells. This accumulation of glutamate and GABA in Müller cells may occur as a result of increased release of these neurotransmitters from neurons, and decreased degradation. Quantification of the semisaturation value (half-maximal response) for glutamate and GABA Müller cell loading during postmortem ischemia indicated a shorter semisaturation value for GABA than glutamate. Such changes are consistent with a single aerobically dependent GABA-degradation pathway, and the existence of multiple glutamate-degradation pathways. Comparison with the in vitro ischemic model showed similar qualitative characteristics, but a markedly increased semisaturation time for glutamate and GABA Müller cell loading (a factor of 5–10) in the postmortem ischemia model. We interpret these differences to indicate that the in vitro condition provides a more immediate and/or severe ischemic insult. In the postmortem ischemia model, the delayed glial cell loading implies the availability of internal stores of both glucose and/or oxygen. Increased glial and neuronal immunoreactivity for the amino acids involved in transamination reactions, aspartate, alanine, leucine, and ornithine was observed, indicating a potential shift in the equilibrium of transamination reactions associated with glutamate production. These findings provide evidence that, in the rat retina, there are multiple pathways subserving glutamate production/degradation that include a multitude of transamination reactions. Further evidence is therefore provided to support a role for all four amino acids in glutamate metabolism within a variety of retinal neurons and glia.

Electrical synapses or gap junctions occur between many retinal neurons. However, in most cases, the gap junctions have not been visualized directly. Instead, their presence has been inferred from tracer spread throughout the network of cells. Thus, tracer coupling is taken as a marker for the presence of gap junctions between coupled cells. AII amacrine cells are critical interneurons in the rod pathway of the mammalian retina. Rod bipolar cell output passes to AII amacrine cells, which in turn make conventional synapses with OFF cone bipolar cells and gap junctions with ON cone bipolar cells. Injections of biotinylated tracers into AII amacrine cells reveals coupling between the AII amacrine cell network and heterologous coupling with a variety of ON cone bipolar cells, including the calbindin-positive cone bipolar cell. To directly visualize gap junctions in this network, we prepared material for electron microscopy that was double labeled with antibodies to calretinin and calbindin to label AII amacrine cells and calbindin-positive cone bipolar cells, respectively. AII amacrine cells were postsynaptic to large vesicle-laden rod bipolar terminals, as previously reported. Gap junctions were identified between AII amacrine cells and calbindin-positive cone bipolar cell terminals identified by the presence of immunostaining and ribbon synapses. This represents direct confirmation of gap junctions between two different yet positively identified cells, which are tracer coupled, and provides additional evidence that tracer coupling with Neurobiotin indicates the presence of gap junctions. These results also definitively establish the presence of gap junctions between AII amacrine cells and calbindin bipolar cells which can therefore carry rod signals to the ON alpha ganglion cell.

Normal photoreceptor cells on the ventral nerve of Limulus respond to a moderately intense flash with a large receptor potential or current. Occasionally, cells are found in which the same flash evokes only a small receptor potential or current. Our investigations reveal physiological reasons for the poor light sensitivity in these “unusual cells.” In unusual cells prolonged illumination with intense light evokes a step-like inward current with an amplitude of some nanoamperes, but without a large transient peak. The current appears to be summed up of single photon responses with amplitudes smaller than about 50 pA. Their time course is similar to that of small single photon responses forming the so-called macroscopic C1 component in normal cells. The macroscopic current evoked by an intense flash has slow activation and deactivation kinetics and reaches a saturated amplitude of about 4–5 nanoamperes. The light-intensity dependence of the current evoked by flashes or by prolonged illumination has a slope of about 1 in log–log plots. The decay kinetics of the current is similar to that of the C1 component measured in normal cells after the block of the C2 component. Occasionally, the step-like current is superposed by large standard bumps. These bumps are blocked by the Ca2+-ATPase inhibitor cyclopiazonic acid, while the sustained inward current persists. We conclude that in unusual cells the light-activated current is identical to the C1 component of normal cells. The phospholipase C pathway that in normal cells presumably gives rise to the C2 component functions only with a low efficiency in unusual cells.