Melatonin biosynthesis in chick retina occurs as a circadian rhythm. Biosynthesis of the neurohormone is highest at night in darkness, and is suppressed by light. The role of gamma-aminobutyric acid (GABA) in the nocturnal regulation of melatonin synthesis was examined. Systemic or intravitreal administration of muscimol, a GABA-A receptor agonist, to light-exposed chicks at the beginning of the dark phase of the light/dark cycle increased retinal melatonin levels and the activity of serotonin N-acetyltransferase (NAT), a key regulatory enzyme of the melatonin biosynthetic pathway. Baclofen, a GABA-B receptor agonist, also increased NAT activity of light-exposed retinas, but muscimol was approximately 40-fold more potent than baclofen. Effects of both muscimol and baclofen on NAT activity were inhibited by GABA-A antagonists, bicuculline and picrotoxin, and the effect of baclofen was unaffected by the GABA-B selective antagonist, CGP 35348. Thus, activation of GABA-A receptors appears to be associated with increased melatonin biosynthesis. The GABA-uptake inhibitor, nipecotic acid, and the GABA-transaminase inhibitor, aminooxyacetic acid, also increased NAT activity of light-exposed retinas. The high levels of NAT activity associated with exposure to darkness were unaffected by either muscimol or baclofen, but picrotoxin and bicuculline significantly inhibited retinal NAT activity in darkness.

The rate of dopamine synthesis, estimated from in situ tyrosine hydroxylase activity, was higher in light-exposed retinas than in darkness. Muscimol inhibited dopamine synthesis in light, and picrotoxin stimulated dopamine synthesis in darkness. The stimulation of melatonin synthesis by muscimol in light-exposed retinas appears to be related to inhibition of retinal dopamine neurons. The increase of NAT activity elicited by muscimol in light-exposed retinas was inhibited by administration of the dopamine receptor agonists apomorphine and quinpirole. Blocking dopamine receptors with spiperone or inhibiting dopamine biosynthesis with α-methyl-ρ tyrosine also increased NAT activity in light, and the effects of the dopamine antagonists and muscimol were not additive. The decrease of NAT activity elicited by GABA antagonists in darkness was inhibited by spiperone. Thus, GABA may indirectly regulate retinal melatonin biosynthesis, by inhibiting dopaminergic activity in retina.

Visually evoked field potentials in human subjects and single-cell responses from retinal ganglion cells in the macaque monkey were compared in closely similar stimulus situations. The classical heterochromatic flicker photometry (HFP) technique was used to measure spectral sensitivity in man, both psychophysically and by recording the 40-Hz response, and to measure the spectral sensitivity of magnocellular (MC-) pathway cells of the macaque. The three measures gave closely similar spectral-sensitivity curves. Close agreement between the three measures was also found when the variable-modulation HFP technique was used to measure spectral sensitivity. When the relative phase between red and green lights was varied, the point of minimum subjective flicker for human observers was close to a sharp minimum found in the amplitude of the 40-Hz response in human and was also close to a minimum in the response of MC-pathway neurons in the monkey. The human 40-Hz response saturated at between 10 and 30% modulation depth, and so did the response of MC-pathway cells in the monkey.

The 16-Hz response in human showed none of the above correlations with MC-pathway properties. On the other hand, parvocellular (PC-) pathway cells responded vigorously to constant-luminance, chromatic modulation, at frequencies higher than can be detected by human observers. The human 16-Hz response also was strong in that stimulus situation. In addition, the response of PC-pathway cells on increasing modulation depth showed little saturation, and this behaviour was paralleled by the human 16-Hz response.

We conclude that the properties of MC-pathway neurons in macaque are closely similar to the properties of the human 40-Hz response in the respects just described. We suggest that the 40-Hz response may offer a means of objectively isolating and investigating the contribution of the magnocellular stream to cortical activity in human. In contrast, the properties of PC-pathway neurons in macaque are quite different from the properties of the human 40-Hz response, and in several respects resemble the properties of the human 16-Hz response.

Cortical projections to the middle temporal (MT) visual area were studied by injecting the retrogradely transported fluorescent tracer Fast Blue into MT in adult New World monkeys (Cebus apella). Injection sites were selected based on electrophysiological recordings, and covered eccentricities from 2–70 deg, in both the upper and lower visual fields. The position and laminar distribution of labeled cell bodies were correlated with myeloarchitectonic boundaries and displayed in flat reconstructions of the neocortex. Topographically organized projections were found to arise mainly from the primary, second, third, and fourth visual areas (V1, V2, V3, and V4). Coarsely topographic patterns were observed in transitional V4 (V4t), in the parieto-occipital and parieto-occipital medial areas (PO and POm), and in the temporal ventral posterior area (TVP). In addition, widespread or nontopographic label was found in visual areas of the superior temporal sulcus (medial superior temporal, MST, and fundus of superior temporal, FST), annectent gyrus (dorsointermediate area, DI; and dorsomedial area, DM), intraparietal sulcus (lateral intraparietal, LIP; posterior intraparietal, PIP; and ventral intraparietal, VIP), and in the frontal eye field (FEF). Label in PO, POm, and PIP was found only after injections in the representation of the peripheral visual field (>10 deg), and label in V4 and FST was more extensive after injections in the central representation. The projections from V1 and V2 originated predominantly from neurons in supragranular layers, whereas those from V3, V4t, DM, DI, POm, and FEF consisted of intermixed patches with either supragranular or infragranular predominance. All of the other projections were predominantly infragranular. Invasion of area MST by the injection site led to the labeling of further pathways, including substantial projections from the dorsal prelunate area (DP) and from an ensemble of areas located along the medial wall of the hemisphere. In addition, weaker projections were observed from the parieto-occipital dorsal area (POd), area 7a, area prostriata, the posterior bank of the arcuate sulcus, and areas in the anterior part of the lateral sulcus. Despite the different nomenclatures and areal boundaries recognized by different models of simian cortical organization, the pattern of projections to area MT is remarkably similar among primates. Our results provide evidence for the existence of many homologous areas in the extrastriate visual cortex of New and Old World monkeys.

We have studied the organization of receptive fields of ganglion cells in the isolated mouse retina and have shown that the organization is similar to that of the cat. Based upon responses to circular and annular stimuli, most ganglion cells (90%; N = 83) had receptive fields with concentric center-surround organization, either ON or OFF center. The plot of response amplitude vs. stimulus area for these cells increased to a maximum (corresponding to a diameter of 10.0 ± 2.8 deg S.E.M.; N = 13) and then decreased for larger stimuli, demonstrating the presence of an antagonistic surround. The dark-adapted sensitivity (205 ± 43.8 impulses quantum−1 rod−1; mean ± S.E.M.) did not differ from that measured for the intact preparation. We found a subset of OFF-center cells for which the dark discharge was very regular (mean coefficient of variation = 0.30). Using sinusoidal grating stimuli, we classified ganglion cells as X-like (87%) and Y-like (13%) based on spatial summation properties and the presence of subunit activity in the receptive-field center. We found no difference in the spatial-frequency preference between X-like and Y-like cells in the central retina (high cutoff frequency, 0.20 ± 0.014 cycle/deg, mean ± S.E.M.), in contrast to the marked difference between X cells and Y cells in the cat. Thus, ganglion cell receptive fields in the mouse retina resemble those of the cat, although the spatial characteristics of the receptive fields in the central retina are more homogeneous. This homogeneity would simplify the comparison of retinas from normal and mutant strains of the mouse.

Studies of form-deprivation myopia (FDM) in animal models have shown that postnatal ocular growth is regulated by the quality of patterned images on the retina. One of the major challenges in myopia research is to identify the biochemical mechanisms which translate retinal visual responses into signals that regulate scleral growth. Dopamine (DA) has been implicated in this process, since retinal DA levels decline in FDM and subconjunctival injections of apomorphine (Apo, a nonspecific DA agonist) prevent FDM in a dose-dependent way (Stone et al., 1989).

To gain insight into where and how DA ligands act to regulate ocular elongation, we compared the action and distribution of DA receptor ligands injected intravitreally vs. subconjunctivally in young chicks. Ocular length was measured by A-scan ultrasound. We found that daily intravitreal injections of Apo block FDM at a 50% effective dose (ED50) of 5 pg per day, or a peak concentration in the vitreous humor of 108 pM, compared to an ED50 of 2.5 ng for subconjunctival injections as reported by Stone et al. (1989, 1990). [3H]-spiperone, a D2-receptor antagonist, reached average maximum retinal concentrations of 160 pM and 260 pM, during the first hour after intravitreal and subconjunctival administration, respectively, at the ED50 dose. In contrast, the maximum spiperone concentrations in the retinal pigment epithelium (RPE) were 30 pM and 410 pM, respectively, after intravitreal or subconjunctival ED50 doses. Spiperone concentrations in sclera after ED50 doses to the two sites differed by 4 x 104 (0.4 pM vs. 1.7 nM, respectively). The FDM-preventing action of Apo was blocked completely by simultaneous administration of spiperone but not by SCH 23390 (a D1-receptor antagonist) in 100-fold molar excess.

These results show that apomorphine acts to prevent FDM at an intraocular site, presumably in retina and/or pigment epithelium, but not sclera, whether administered intravitreally or subconjunctivally. A dose yielding a concentration of 100–260 pM, delivered ≤1 h per day, produces half-maximal inhibition. This action is mediated by D2-receptors, for which the dissociation constant for apomorphine is ≤1 nM. The retinal pigment epithelium may act as a trophic relay station, responding to a retinal messenger which may be DA and secreting scleral growth-regulator(s) from its basal surface.

We recorded the responses of neurons from the cat’s lateral geniculate nucleus to drifting sine-wave grating stimuli both before and during electrical stimulation of the parabrachial region of the midbrain. The parabrachial region provides a mostly cholinergic input to the lateral geniculate nucleus, and our goal was to study its effect on responses of geniculate cells to visual stimulation. Geniculate neurons respond to visual stimuli in one of two modes. At relatively hyperpolarized membrane potentials, low threshold (LT) Ca2+ spikes are activated, leading to high-frequency burst discharges (burst mode). At more depolarized levels, the low threshold Ca2+ spike is inactivated, permitting a more tonic response (relay or tonic mode). During our intracellular recordings of geniculate cells, we found that, at initially hyperpolarized membrane potentials, LT spiking in response to visual stimulation was pronounced, but that parabrachial activation abolished this LT spiking and associated burst discharges. Coupled with the elimination of LT spiking, parabrachial activation also led to a progressive increase in tonic responsiveness. Parabrachial activation thus effectively switched the responses to visual stimulation of geniculate neurons from the burst to relay mode. Accompanying this switch was a gradual depolarization of resting membrane potential by about 5–10 mV and a reduction in the hyperpolarization that normally occurs in response to the inhibitory phase of the visual stimulus. Presumably, the membrane depolarization was sufficient to inactivate the LT spikes. We were able to extend and confirm our intracellular observations on the effects of parabrachial activation to a sample of cells recorded extracellularly. This was made possible by adopting empirically determined criteria to distinguish LT bursts from tonic responses solely on the basis of the temporal pattern of action potentials. During parabrachial activation, every cell responded only in the relay mode, an effect that corresponds to our intracellular observations. We quantified the effects of parabrachial activation on various response measures. The fundamental Fourier response amplitude (Fl) was calculated separately for the total response, the tonic response component, and the LT burst component. Parabrachial activation resulted in an increased Fl amplitude for the total response. This increase was due to an increase in the tonic response component. For a subset of cells showing epochs of LT bursting, parabrachial activation concurrently reduced LT bursting and increased the amplitude of the tonic response. Parabrachial activation, by eliminating LT bursting, also caused cells to respond with more linearity. By keeping geniculate cells in the relay mode, the parabrachial region serves to maintain a more linear retinogeniculate transfer of information to cortex, and this may be important for detailed analysis of visual targets. However, when a geniculate neuron becomes hyperpolarized, as may occur during states of visual inattention, it would not respond well to visual stimuli without the sort of nonlinear amplification provided by the LT spike. Thus, the LT spike may permit hyperpolarized cells to relay to cortex the presence of a potentially salient or dangerous stimulus, but this is done at the expense of linearity. This may serve as a sort of “wake-up call” that redirects attention to a particular stimulus and eventually enhances activity of appropriate parabrachial inputs to switch the critical geniculate neurons into the relay mode.

Cytochrome-oxidase (CO) histochemistry has revealed important functional subdivisions, modules, and processing streams in the macaque visual cortex. The present study is aimed at analyzing the development and characteristics of CO patterns in the human visual cortex by means of histochemistry and immunohistochemistry. At 26 weeks of gestation, both the ventricular and subventricular zones had low levels of CO, while the cortical plate had moderate levels of CO. At birth, supragranular CO-rich zones (puffs) were not clearly organized, indicating that the development of puffs in the neonatal striate cortex lags behind that of the macaque monkey, whose puffs appear weeks before birth. Puffs were more clearly discernible in human cortex at postnatal day 24, and became well organized by the fourth postnatal month. Layer IVcα in the neonate exhibited a higher level of activity and amount of CO than the central portion of IVcβ, which contained a dense aggregate of small neurons. The base of IVcβ, however, was often as CO reactive as IVcα. In contrast, the majority of specimens available to us from the fourth postnatal month and from adults with no known neurological diseases had significantly greater CO reactivity in layer IVcβ than in IVcaβ. Layer VI was moderately reactive for CO throughout development. In V2, stripes with globular zones of high CO activity were sporadically present at birth, suggesting that their development may parallel or precede that of puffs in VI. These stripes with CO-rich globular zones became more prominent in the adult and radiated orthogonally from the V1/V2 border. They were not, however, clearly organized into alternating thick and thin stripes as they are in the squirrel monkey. Visual cortical areas beyond V2 exhibited high CO activity mainly in layers III and IV and moderate levels in VI, suggesting that sites associated with cortico-cortical pathways may be metabolically most active.

The results of previous studies suggest that class-specific interactions contribute to the development of the different classes of retinal ganglion cells. We tested this hypothesis by examining the morphologies and distributions of alpha (α) cells in regions of mature cat retina selectively depleted of beta (β) cells as a result of visual cortex lesions at birth. We find that α cells in regions of central retina depleted of β cells are abnormally large while α cells in regions of peripheral retina depleted of β cells are abnormally small. The normal central-to-peripheral α cell soma-size gradient is absent in hemiretinae depleted of β cells. The dendritic fields of α cells in the border of β-cell-depleted hemiretina extend preferentially into the β-cell-poor hemiretina. In spite of this, α cell bodies retain their normal retinal distribution and remain distributed in a nonrandom mosaic-like pattern. Thus, it appears that the development of α retinal ganglion cells is influenced by interactions both with other α cells (class-specific interactions) and with surrounding β cells (nonclass-specific interactions).

The leading edge of the a–wave of the electroretinogram (ERG) was evaluated as a measure of human cone photoreceptor activity. The amplitude of the cone a–wave elicited by flashes of different energy was compared to the predictions of a class of models from in vitro studies of cone photoreceptors. These models successfully describe the leading edge of the a–wave. Thus, the human cone a–wave can be used to test hypotheses about normal and abnormal cone receptors. The ability of the human cone to adjust its sensitivity in the presence of steady adapting lights was assessed by recording cone a–waves to flashes on adapting fields up to 3.9 log td in intensity and by comparing these responses to quantitative models of adaptation. The first 10 ms of the cone's response is little affected by field intensities up to 2.9 log td. The 3.9 log td field reduced the response to weak flashes by about a factor of 2.5 (0.4 log unit). This relatively small reduction in sensitivity can be attributed to a combination of response compression, pigment bleaching, and an adaptation mechanism that changes the gain without changing the time course. We conclude that either the human cones show relatively little adaptation or that they have an adaptation mechanism that involves a time-course change. That is, as we are limited with the a–wave to the first 10 ms or so of the cone's response, we cannot rule out a gain mechanism linked to a time-course change.

Previous studies indicate that cortical areas 17 and 18 play a prominent role in generating the direction selectivities of neurons in the superior colliculus of the cat. This hypothesis was tested by quantifying the activities of neurons in the superficial collicular layers in intact cats and cats which incurred ablation of areas 17 and 18 and part of area 19. In addition, since behavioral and anatomical studies suggest a functional adjustment in the superior colliculus following removal of inputs from areas 17, 18, and 19 in the neonatal cat, we included a group of neonatally lesioned cats. Computation of an index of directionality indicated that the majority of neurons in intact cats preferred movement in one direction, thus confirming reports of others. Following ablation of areas 17 and 18 and part of area 19 in both groups of lesioned cats, only modest changes in the population indices were detected when poorly responsive neurons were eliminated from the analyses. Based upon levels of visually evoked neuronal activity, our data suggest a physiological compensation by neurons in stratum griseum superficiale following removal of areas 17, 18, and 19 inputs. In the intact and neonatally operated groups, activity in stratum griseum superficiale is high, whereas in the adult lesioned group activity is low. In stratum opticum, neuronal activity was similar in all three groups of cats. These results show that neurons in stratum griseum superficiale undergo a physiological compensation following removal of immature areas 17 and 18.

We recorded optokinetic eye movements of the crab, Carcinus maenas, in split-drum experiments. The patterns were either oscillated in antiphase on both sides mimicking translational image flow or they were oscillated in phase producing rotational image flow. Eye movements elicited by the rotational stimulus were larger than those produced by the pseudotranslational pattern movements. The smaller response to the latter is mainly a consequence of binocular interaction, the strength of which depends on both the phase-shift and amplitude of pattern oscillation. We develop two hypotheses to explain our results: either (1) signals from each eye modify the gain of the linkage signals coming from the other eye, or (2) the signals coming from the other eye modify the gain of the control loop itself. Quantitative evaluation of the data favors the second of these two hypotheses, which comprises the models of Barnes and Horridge (1969) and Nalbach et al. (1985). In addition, we found that it is the signals from the two slow channels of the crab's movement-detecting system that are transferred from one eye to the other, while signals of the fastest channel act almost exclusively ipsilaterally. We discuss our results as an adaptation by which an animal with panoramic vision compensates exclusively the rotational component of image flow during locomotion. The fact that freely walking crabs distinguish the two components of image flow better than restrained crabs indicates that further visual and nonvisual signals help to disentangle image flow.

Although serotonin is thought to be a neurotransmitter in a number of retinal systems, much of the precise synaptic connectivity of serotonergic neurons is unknown. To address this issue, we used an antiserum directed against serotonin to label serotonergic bipolar and amacrine cells in the turtle retina. Light-microscopic analysis of labeled amacrine and bipolar cells indicated that both had bistratified dendritic arborizations primarily in stratum 1 and in strata 4/5 of the inner plexiform layer.

Ultrastructural analysis of the neurocircuitry of these cells indicated that the processes of labeled bipolar cells in the outer plexiform layer made basal junction contacts with photoreceptor terminals. Only in rare instances did labeled bipolar cells processes invaginate near photoreceptor ribbon synapses. Processes of labeled bipolar cells received both conventional and small ribbon synaptic contacts in the outer plexiform layer. Bipolar cell processes in stratum 1 of the inner plexiform layer synapsed onto either amacrine/amacrine or amacrine/ganglion cell dyads, and made rare ribbon synaptic contacts onto labeled amacrine cell processes. Synaptic inputs to serotonergic bipolar cells in stratum 1 were from unlabeled bipolar and amacrine cells. Bipolar cell contacts in strata 4/5 were similar to those in stratum 1, but were fewer in number and no bipolar cell inputs were seen.

Labeled amacrine cell output in both strata was onto other unlabeled amacrine cells and ganglion cells; but synaptic outputs to unlabeled bipolar cells were only seen in strata 4/5. In both strata 1 and 4/5, synaptic inputs to labeled amacrine cells were from both unlabeled amacrine cells and labeled bipolar cells. The serotonergic amacrine cells had many more synaptic interactions in stratum 1 than in strata 4/5 which supports the role of serotonergic bipolar cells in the OFF pathway of retinal processing. Interactions between serotonergic bipolar and amacrine cells may play an important role in visual processing.

To investigate the subcortical connections of the object vision and spatial vision cortical processing pathways, we injected the inferior temporal and posterior parietal cortex of six Rhesus monkeys with retrograde or anterograde tracers. The temporal injections included area TE on the lateral surface of the hemisphere and adjacent portions of area TEO. The parietal injections covered the posterior bank of the intraparietal sulcus, including areas VIP and LIP. Our results indicate that several structures project to both the temporal and parietal cortex, including the medial and lateral pulvinar, claustrum, and nucleus basalis. However, the cells in both the pulvinar and claustrum that project to the two systems are mainly located in different parts of those structures, as are the terminals which arise from the temporal and parietal cortex. Likewise, the projections from the temporal and parietal cortex to the caudate nucleus and putamen are largely segregated. Finally, we found projections to the pons and superior colliculus from parietal but not temporal cortex, whereas we found the lateral basal and medial basal nuclei of the amygdala to be reciprocally connected with temporal but not parietal cortex. Thus, the results show that, like the cortical connections of the two visual processing systems, the subcortical connections are remarkably segregated.

Experiments on the lateral geniculate nucleus (LGN) of the cat based on 14C 2-deoxyglucose (2-DG) autoradiography and intraocular injections of 2-amino-4-phosphonobutyric acid (APB) provided evidence for gradients of metabolic activity in the ON and OFF pathways in layer A, but only very weakly, if at all, in layer Al. Alert and freely moving cats were exposed to square-wave gratings over a 45-min period after injection of the 2-DG. When one eye had been treated previously with APB, contralateral layer A showed a clear gradient of 2-DG label indicating that the remaining OFF pathway was most active ventrally in the layer and, by implication, that the ON pathway is normally most active dorsally. No gradient was apparent in layer Al ipsilateral to the APB eye. Control experiments based on binocular injections of tetrodotoxin (TTX) demonstrated that no gradients were present in the baseline activity within the layers. Finally, monocular injections of TTX provided evidence for gradients of nondominant eye activity in layers A and Al that were maximal near the interlaminar zone between layers A and A1 and declined in mirror-symmetric fashion toward the dorsal border of A and the ventral border of A1.

Combined with earlier anatomical studies showing depth-dependent patterns of geniculo-cortical projection, these results indicate that in the cat, as in several other species, the visual input to striate cortex is partly organized around ON and OFF pathways. In addition, the results suggest that a systematic variation of binocular interaction, perhaps related to ocular dominance, exists through the depths of the geniculate layers. Understanding how the ON and OFF pathways, and binocular interactions, are organized in the thalamus may provide insight into the functional merging of these systems in the cortex.

We evaluated the subcortical pathways’ contribution to human adults’ horizontal OKN by using a method similar to that used previously with cats (Harris & Smith, 1990; Smith & Harris, 1991). Five normal adults viewed plaids composed of two drifting sinusoidal gratings arranged such that their individual directions of drift were 60 deg or more from the direction of coherent motion of the overall pattern. Physiological evidence indicates that under monocular viewing, nasalward coherent motion gives advantage to any crossed subcortical contribution while temporalward coherent motion minimizes it. We recorded horizontal eye movement by infrared reflection and asked subjects to report the perceived direction of motion.

During both binocular and monocular viewing, the direction of the slow phase of OKN fell closer to the direction of coherent movement than to that of the oriented components. Monocular viewing produced no nasal-temporal asymmetries in the influence of coherent motion on the direction of OKN. This suggests that in humans the influence of coherent motion is mediated primarily by cortical mechanisms and, unlike in cats, with little or no involvement of subcortical mechanisms in the generation of horizontal OKN.

Walking crabs move their eyes to compensate for retinal image motion only during rotation and not during translation, even when both components are superimposed. We tested in the rock crab, Pachygrapsus marmoratus, whether this ability to decompose optic flow may arise from topographical interactions of local movement detectors. We recorded the optokinetic eye movements of the rock crab in a sinusoidally oscillating drum which carried two 10-deg wide black vertical stripes. Their azimuthal separation varied from 20 to 180 deg, and each two-stripe configuration was presented at different azimuthal positions around the crab. In general, the responses are the stronger the more widely the stripes are separated. Furthermore, the response amplitude depends also strongly on the azimuthal positions of the stripes. We propose a model with excitatory interactions between pairs of movement detectors that quantitatively accounts for the enhanced optokinetic responses to widely separated textured patches in the visual field that move in phase. The interactions take place both within one eye and, predominantly, between both eyes. We conclude that these interactions aid in the detection of rotation.

In previous experiments we established that a light flash reduced cGMP levels of toad rod outer segments within the transduction time interval, but that recovery of the dark level of cGMP occurred more slowly than reported electrophysiological recovery of membrane potential. We now report that a second light flash accelerates the recovery rate of total cGMP following an initial flash, but that this acceleration is blocked in a medium which is both sodium and calcium deficient. We also noted that calcium deficiency only elevated cGMP levels when sodium was present. For other experiments, we recorded ERG or aspartate isolated PIII responses from eyecups or retinas mounted on our quick-freeze apparatus, the light stimuli originating from the double light-bench of the latter. Whereas background illumination depressed cGMP, no detectable further cGMP loss accompanied the electrical response to a flash superimposed on the background.

In the turtle retina, dopamine has been observed in a small population of amacrine cells. Whereas the effect of dopamine has been intensively studied, knowledge about the release of this transmitter and the neuronal control of its release are still poorly understood. We therefore decided to study the release of endogenous dopamine. Isolated retinas were superfused with Ringer’s solutions and stimulated with increased potassium, light, or drugs which interfere with neurotransmitter systems. Dopamine was analyzed by using aluminum-oxide extraction and high-pressure liquid chromatography (HPLC) with electrochemical detection. Increased potassium (25 mM) caused a five-fold increase in the basal release. When calcium was replaced by cobalt, no increase was induced by 25 mM potassium. Flickering light increased the basal release of endogenous dopamine by a factor of three. The effect of flickering light was greater in the presence of additional steady background illumination. Kainate (10 μM), an agonist for excitatory amino acids, doubled the basal dopamine release. Bicuculline (10 μM), a γ-amino butyric acid (GABA) antagonist, increased the release to about six times the basal level. Naloxone (10 μM), an opiate antagonist, increased the release to eight times the basal level. These findings suggest that dopamine is released from amacrine cells in the turtle retina in a calcium-dependent manner, which is most likely a vesicular release. Dopamine release is induced by flickering light vs. darkness and vs. steady background illumination. A moderate background illumination alone does not significantly increase basal dopamine release. Drug treatment during the release experiments suggests that dopaminergic neurons receive an excitatory input either directly or indirectly from glutamatergic bipolar and/or amacrine cells and inhibitory inputs either directly or indirectly from GABAergic amacrine cells and from enkephalinergic amacrine cells or efferent fibers.

We investigated the attributes of transduction and light-adaptation in rods, single cones, and twin cones isolated from the retina of striped bass (Morone saxatilis). Outer-segment membrane currents were measured with suction electrodes under voltage clamp provided by tight-seal electrodes applied to the cell’s inner segment. Brief flashes of light transiently reduced the outer-segment current with kinetics and sensitivity characteristic of each receptor type. In all cells, the responses to dim lights increased linearly with light intensity. The amplitude-intensity relation for rods and single cones were well described by an exponential saturation function, while for twin cones it was best described by a Michaelis-Menten function. At the wavelength of maximum absorbance, the average intensity necessary to half-saturate the peak photocurrent in dark-adapted rods was 28 photons/μm2 and in single cones it was 238 photons/μm2. Among twin cones, the common type (88% of all twins recorded) half-saturated at an average of 1454 photons/μm2, while the fast type reached half-saturation at an average of 9402 photons/μm2. The action spectrum of the photocurrent in the three receptor types was well fit by a nomogram that describes the absorption spectrum of a vitamin A2-based photopigment. The wavelength of maximum absorbance for rods was 528 nm, for single cones it was 542 nm and for twin cones it was 605 nm. Both members of the twin pair contained the same photopigment and they were electrically coupled. Under voltage clamp, the response to dim flashes of light in both single and twin cones was biphasic. The initial peak was followed by a smaller amplitude undershoot. Single cones reached peak in 86 ms and common twins in 50 ms. Background light desensitized the flash sensitivity in all photoreceptor types, but was most effective in rods and least effective in fast twins. In the steady state, the desensitizing effect of a background intensity, Ib, at the respective optimum wavelength for each cell was well described by the Weber-Fechner law (1/(1 + Ib/Ibo)), where Ibo was, on average (in units of photons/μm2/s), 1.45 for rods, 1.81 x 103 for single cones, 4.56 x 103 for common twins, and 6.79 x 104 for fast twins.

We have described the currents flowing across the presynaptic membranes of the four median photoreceptors of the giant barnacle, Balanus nubilus, using a quasi-voltage clamp arrangement. Membrane potential, measured in the terminal region of one photoreceptor, was controlled in all four terminals by feedback current supplied through the nerve containing the photoreceptors’ axons. The [Ca2+] ∘ in the saline was reduced to decrease the Ca2+ current, enabling better voltage control, and tetraethylammonium ion (TEA, 20 mM) was added to block a fast voltage-dependent K+ conductance.

Depolarizing voltage steps from the resting potential in the dark (−60 mV) evoked slow, inward Ca2+-dependent currents which could be blocked by Co2+, Mg2+, or Cd2+. The Ca2+ currents were followed by large outward currents that persisted for many seconds after the offset of moderate or large pulses. These tail currents increased in magnitude and duration with pulse duration and reversed at about −80 mV, consistent with previous evidence for a Ca2+-activated K+ conductance in this membrane. When the Ca2+-activated outward current was reduced to zero by increasing the [K+]∘ so as to set EK at −20 mV, and then stepping the voltage to this value, the step evoked a steady inward Ca2+ current. Thus, the Ca2+ current did not show voltage- or Ca2+-dependent inactivation. When Ba2+ was substituted for Ca2+, 500-ms depolarizing steps evoked steady inward currents but no outward currents. In any given experiment, the activation voltage of the Ca2+ or Ba2+ current did not depend on holding potential.

At the barnacle photoreceptor’s synapse, the postsynaptic cell adapts to maintained presynaptic voltage by a mechanism that is not understood. We conclude that neither Ca2+ current inactivation nor a shift in activation voltage with holding potential can account for this adaptation.