Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter used by many neurons of the mammalian retina. To identify the synaptic targets of these cells, we undertook an immunohistochemical study with a monoclonal antibody that recognizes the GABAA receptors (62−3G1, generously donated by A. de Blas). This antibody labels the somata of at least one group of amacrine cells in the inner nuclear layer. It also labels two groups of somata in the ganglion cell layer: one small and the other much larger. The small cells are likely to be displaced amacrine cells based on their size, although some could be gamma ganglion cells. The much larger receptor-positive cells are clearly ganglion cells, based both on their size and the antibody labeling of the initial portion of their axon. In the peripheral retina, the size of these large somata suggests that many are beta ganglion cells. However, at any point across the retina the density of these cells never exceeded 50% of the density of beta cells as a whole.

The antibody also labels a dense plexus of processes that extends throughout the inner plexiform layer (IPL), with a marked concentration in the inner third of the layer. This is the portion of the IPL in which the rod bipolar cells terminate. It is difficult to recognize processes of individual cells in the IPL, so retinae were dissociated. The rod bipolar cells were identified by protein kinase C immunoreactivity (Negishi et al., 1988; Karschin & Wässle, 1990). They were not labeled by the GABAA receptor antibody. This is surprising in light of tight-seal, whole cell voltage-clamp recordings that have shown that the rod bipolars express functional GABAA receptors. One possible explanation is that the antibody recognizes only a subset of the GABAA receptors.

Ocular hypopigmentation is associated with neurological defects in structure and function. This paper investigates the ab/Fute visual thresholds in dark-adapted hypopigmented animals compared to their normally pigmented controls. Here we asked (1) whether the threshold elevation found in hypopigmented animals is a general consequence of the reduction in melanin content; (2) if so, which melanin components in the eye are likely to influence visual thresholds; and (3) whether similar threshold defects can be detected in orders other than rodents. By single-unit recordings from the superior colliculus, we compared incremental thresholds of normal black mice of the C57BL/6J strain to hypopigmented mutants: beige (bg/bg), pale ear (ep/ep), and albino (c2J/c2J) mice, three mutants in which melanin pigment throughout the body is affected; and Steel (Sl/Sld) and dorninant-spotting/W-mice (W/Wν), two mutants with normal pigmentation in the retinal pigment epithelium (RPE) but without any melanin in the choroid or the rest of the body. We found that all mutants had elevated thresholds that varied with the reduction in melanin. The albinos were 25 times less sensitive than black mice, pale ear mice 20 times, beige mice 11 times, and Steel and W-mice 5 times. The mean thresholds of dark-adapted black mice were 0.008 cd/m2. Recordings from rabbits showed a similar impairment of visual sensitivity: incremental thresholds were elevated 40 times in New Zealand-White albino rabbits (0.0008 cd/m2) compared to Dutch-Belted pigmented controls (0.00002 cd/m2). Previously, it has been shown that hypopigmented rats have elevated dark-adapted thresholds compared to pigmented controls (Balkema, 1988); here we show that the difference between hypopigmented rats and pigmented controls is not caused by insufficient dark adaptation or excessive variability in the results from albino mutant compared to its control.

Mutations that cause a reduction of ocular melanin pigmentation, regardless of the gene mutated or the mechanism underlying the hypopigmentation, are accompanied by an elevation in visual thresholds which is roughly proportional to the reduction in melanin. Melanin both in the RPE and choroid exert an effect on visual thresholds. Like the defects in optic nerve crossing and eye movements, the effect of melanin on visual thresholds is not restricted to rodents, but is seen in other orders. The threshold impairment in hypopigmented animals cannot be explained by impaired photoprotection, but it points to another physiological action of melanin.

The lateral suprasylvian (LS) area (or Clare-Bishop area) is a region of visual cortex in the cat which has been defined as an isolated projection zone of area 17 (VI or striate cortex) within the suprasylvian sulcus. We have studied the overall topography and detailed pattern of connection between these two visual areas following injections of WGA-HRP into one or the other.

The projection from area 17 to LS is formed largely (-90%) from supragranular layer neurons that are distributed, in the coronal plane, in multiple regularly spaced patches. These patches are especially prominent in regions of area 17 representing central vision along and around the horizontal meridian. In reconstructions of serial coronal sections, and in flatmounts of the same region, the patches are seen to align so that in the plane tangential to the cortical surface they appear as a system of parallel bands whose main axis of elongation is rostro-ventral to caudo-dorsal, or near parallel to the area 17/18 border. The mean periodicity of the bands is about 1.0 mm.

The projection from area 17 terminates mainly in layers 4, 3, and 2 of area LS, and also appears patchy in the coronal plane. Reconstruction of the cortical surface view again reveals a system of rostrocaudal bands, but with a mean periodicity of 2 mm. The back projection is less periodically organized, arising predominantly (-80%) from a continuous sheet of infragranular neurons in area LS and terminating mainly in layer 1 of area 17, across the underlying patch and interpatch zones of the supragranular projection cells. However, neurons in layers 2 and upper 3 of area LS, which form the minority origin of the back projection, are mostly located in columnar registration with the patches of area 17 terminals.

The bands of supragranular layer neurons projecting to area LS are aligned obliquely to the iso-orientation domains of area 17, indicating a further component to its organization. It is suggested that this may correspond to a segregation of the X and Y channels in area 17, with outputs to area LS selectively arising from the Y pathway, in accordance with previous reports.

Ganglion cell activity in response to drifting or alternating stimulus patterns was recorded in an eyecup preparation of the turtle. The stimuli were sinusoidal gratings with various spatial frequencies and spatial phases. Spike histograms of the activity were Fourier-analyzed. The results indicated that the retinal circuitry always functioned in a nonlinear manner. The average, first, and second harmonics of the activity were all a function of stimulus conditions, including spatial phase. Similar outcomes were obtained with full-field (retina-wide) and a small-field (1 mm diameter) stimulation. In the middle of the spatial-frequency range, the ratio of second to first harmonic activity was higher in response to static, contrast-reversing gratings than for drifting, constant-contrast ones. The findings suggest that, as distinct from the usual X, Y, and W segregation of ganglion cell properties in other retinas, there is a single class of cells whose responses seem to have attributes of one or another of the usual categories depending on stimulus characteristics. This may be the result of a degree of stimulus-dependent functional modification in the retinal input circuitry to the turtle ganglion cells.

Two morphologically distinct types of preganglionic endings are observed in the avian ciliary ganglion: boutonal and cap-like. Boutonal endings synapse on ciliary ganglion neurons (called choroidal neurons) innervating choroidal blood vessels, while cap-like endings synapse on ciliary ganglion neurons (called ciliary neurons) controlling the lens and pupil. Some of both types of preganglionic endings contain the neuropeptides substance P (SP) and/or leucine-enkephalin (LENK). Although both types of preganglionic terminals are also known to be cholinergic, there has been no direct evidence that SP and LENK are found in cholinergic endings in the ciliary ganglion. The present studies in pigeons, which involved the use of single- and double-label immunohistochemical techniques, were undertaken to examine this issue, as well as to (1) determine the relative percentages of the boutonal and cap-like endings that contain SP, LENK, or both SP and LENK; and (2) determine if the two different types of terminals in the ciliary ganglion arise from different subdivisions of the nucleus of Edinger-Westphal (EW).

Single- and double-label immunohistochemical studies revealed that all neurons of EW, regardless of whether they contained immunohistochemically detectible amounts of SP or LENK, are cholinergic. In the medial subdivision of EW (EWM), which was found to contain approximately 700 neurons, 20.2% of these neurons were observed to contain both SP and LENK, while 11.6% were observed to contain SP only and 10.7% were observed to contain LENK only. In contrast, in lateral EW (EWL), which was found to contain approximately 500 neurons, 16.2% of the neurons were observed to contain both SP and LENK, while 19.2% of the neurons were observed to contain SP only and 12.6% were observed to contain LENK only. Retrograde-labeling studies involving horseradish peroxidase injections into the ciliary ganglion revealed that EW was the sole source of input to the ciliary ganglion and all, or nearly all, neurons in EW innervate the ciliary ganglion.

Immunohistochemical labeling of the ciliary ganglion neurons with an antiserum against choline acetyltransferase revealed that approximately 900 choroidal neurons and approximately 600 ciliary neurons are present in the ganglion, all of which receive cholinergic preganglionic endings. Of the choroidal neurons, 94% receive butonal terminals containing both SP and LENK, while only 2% receive SP+ only boutonal endings and 2% receive LENK+ only butonal endings. Of the ciliary neurons, 25% receive cap-like endings containing both SP and LENK, 30% receive cap-like endings containing only SP and 3% receive cap-like endings containing only LENK. Total unilateral lesions of EW resulted in the loss of all SP+ or LENK+ terminals in the ipsilateral ganglion. Subtotal EW lesions that spared either part of EWM or part of EWL revealed that boutonal endings arise from EWM neurons and cap-like endings from EWL neurons.

The present results suggest that the choroidal neurons, which regulate choroidal blood flow, may be relatively uniform in their functional properties since they nearly all receive boutonal endings from EWM that co-contain SP, LENK, and acetylcholine. In contrast, the ciliary neurons, which receive their preganglionic input from EWL, may consist of at least three major functionally distinct subgroups: (1) those receiving SP/LENK/acetylcholine-containing cap-like endings; (2) those receiving SP/acetylcholine-containing cap-like endings; and (3) those receiving acetylcholine-containing cap-like endings. The functional diversity of ciliary neurons may in part be related to the fact that some ciliary neurons innervate the iris and others the ciliary body.

We have produced and characterized a monoclonal antibody, AT101, which selectively labels both viable and formaldehyde-fixed horizontal cell axon terminals, but not their somas or axons, of the goldfish (Carassius auratus) retina. The antigen recognized by AT101 appears to be a cell surface glycoprotein with a molecular weight of about 35,000 Daltons, and is present exclusively or predominantly in nervous tissues of all vertebrate species examined. We have used AT101 as a probe to analyze immunocytochemically the organization of horizontal cell axon terminals (HCATs) in the adult goldfish retina, and the emergence and maturation of these terminals during retinal development. Because of continued growth at the retinal margin in adult goldfish, there is a peripheral-to-central gradient in the age of cells, with the most mature in the center and the youngest in the periphery. In the center and near periphery of the adult retina, HCATs have a fusiform morphology and form a dense network in the middle and proximal part of the inner nuclear layer. In the far peripheral retina, the axon terminals appear round or ellipsoid. The retina closest to the retinal margin is devoid of AT101 staining, indicating that either HCATs are absent or the antigen recognized by AT101 is not present on HCATs at this stage. A similar sequence of changes in staining pattern is seen during development. Although AT101 staining can first be demonstrated in the larval retina at 1 month after hatching, it appears mostly as punctate structures. At a later stage, there are round or ellipsoid structures that resemble in morphology and location (in the inner nuclear layer) those found in the far peripheral adult retina. Double-labeling experiments with AT101 and antiserum against tubulin also indicate that AT101 labels the HCATs when they first appear during development. These data suggest that the emergence and maturation of HCAT is a late event in retinal development.

We report psychophysical evidence for a categorical dichotomy in the perception of contrast. Observers were required to rate the contrast of sinusoidal gratings (2.3 c/d) with contrast varying over a given range relative to two standards. One standard was designated “high” contrast and the other was designated “low.” There was a boundary effect: contrast judgment depended upon whether the tested ranges included 10–15% contrast and discrimination was sharpest at the boundary between 10 and 15% contrast. These results are consistent with the existence of two systems underlying perceived contrast; one primarily sensitive below 10%, and the other primarily sensitive above 15% contrast.

The response amplitude of cat striate cortical cells is usually reduced after exposure to high-contrast stimuli. The temporal characteristics and contrast sensitivity of this phenomenon were explored by stimulating cortical cells with drifting gratings in which contrast sequentially incremented and decremented in stepwise fashion over time. All responses showed a clear hysteresis, in which contrast gain dropped on average 0.36 log unit and then returned to baseline values within 60 s. Noticeable gain adjustments were seen in as little as 3 s and with peak contrasts as low as 3%. Contrast adaptation was absent in responses from LGN cells. Adaptation was found to depend on temporal frequency of stimulation, with greater and more rapid adaptation at higher temporal frequencies. Two different tests showed that the mechanism controlling response reduction was influenced primarily by stimulus contrast rather than response amplitude. These results support the existence of a rapid and sensitive cortically based system that normalizes the output of cortical cells as a function of local mean contrast. Control of the adaptation appears to arise at least in part across a population of cells, which is consistent with the idea that the gain control serves to limit the information converging from many cells onto subsequent processing areas.

We examined the grating acuity and contrast sensitivity of cats whose eye position was monitored with a scleral search-coil technique. During each trial, the cat was required to maintain fixation on a laser spot and respond to the presence or the absence of a grating by pressing a right or left pedal. With this procedure, acuity was measured along the horizontal and vertical meridian over a range of eccentricities in the nasal, temporal, superior, and inferior retina. In addition, contrast sensitivity for stationary and drifting gratings was measured for the temporal retina along the horizontal meridian. Acuity in area centralis reached about 3.5 cycle\deg and declined by 0.5 octaves at 4 deg and by about 1.3 octaves at 16-deg eccentricity in the nasal retina. The acuity was higher in the nasal than temporal retina. At all eccentricities, spatial resolution exceeded the resolution limit derived from Y (alpha)-cell properties. Contrast sensitivity also decreased as the eccentricity increased when the target size was held constant. The slope of sensitivity-eccentricity function was relatively shallow for a low spatial frequency (0.30 cycle\deg) with sensitivity decreasing by a factor of 1.5–2 at 8-deg eccentricity. The slope of the sensitivity falloff for high spatial-frequency gratings (1.2 cycle\deg) was steeper, with a 5–10-fold difference in sensitivity between 0 and 8 deg. By varying the target size, we determined that the summation area in the cat is about a factor of 3 smaller in area centralis than a 16-deg eccentricity. When the size of the centrally and peripherally viewed targets was scaled relative to visual acuity, the sensitivity was constant across the visual field.

Evidence is presented that innate microstrabismus and abnormal cortical visual receptive-field properties can occur also in cats without any apparent involvement of the Siamese or albino genetic abnormalities in their visual system. A possible cause for microstrabismus in these cats may be sought in an abnormally large horizontal distance between blind spot and area centralis indicated by a temporal displacement of the most central receptive fields on both retinae.

Depth perception was found to be impaired in cats with innate microstrabismus. Behavioral measurements using a Y-maze revealed in four such cats that the performance in recognizing the nearer of two random-dot patterns did not improve when they were allowed to use both eyes instead of only one. The ability of microstrabismic cats to perceive depth under binocular viewing conditions only corresponded to the monocular performance of five normal cats.

Electrophysiological recordings were performed in the visual cortex (areas 17 and 18) of four awake cats, two normal, and two innate microstrabismic animals. Ocular dominance and orientation tuning of single neurons in area 17 and 18 were analyzed quantitatively.

The percentage of neurons in area 17 and 18 which could be activated through either eye was significantly reduced to 49.7% in the microstrabismic animals when compared to the normal cats (74.8%). “True binocular cells,” which can only be activated by simultaneous stimulation of both eyes, were significantly less frequent (1.6%) in microstrabismic cats than in normal animals (10.4%). However, subthreshold binocular interactions were identical in both groups of animals. In the strabismic animals, long-term binocular stimulation of monocular neurons did not give a clear indication of alternating use of one or the other eye.

The range of stimulus orientations leading to discharge rates above 50% of the maximal response, i.e. the half-width of the orientation tuning curves, was the same in the two groups of cats. However, orientation sensitivity, i.e. the alternation in discharge rate per degree change in stimulus orientation, was higher in cortical cells of normal cats than in those of microstrabismic cats.

In normal and microstrabismic cats, no clear sign of an “oblique effect,” i.e. the preference of cortical neurons for vertical and horizontal orientations compared to oblique orientations, could be found neither in the incidence of cells with horizontal or vertical preferred orientation nor in the sharpness of orientation tuning and sensitivity of these neurons.

In summary, the receptive-field properties reported here for awake innate microstrabismic cats are similar to those reported in the literature for anesthetized cats with varying degrees of albinism and for cats with artificial symmetrical strabismus surgically induced by sectioning the equivalent extraocular muscles in both eyes. Our innate microstrabismic cats may provide, however, an animal model for investigating the etiology of one form of naturally occurring strabismus.

Previous studies have reported that the surround responses of retinal ganglion cells weaken or disappear upon dark adaptation. The mechanism(s) by which this occurs is largely unknown, although changes in activity of retinal dopaminergic neurons have been implicated. In the light-adapted rabbit retina, the surround ON responses of OFF-center ganglion cells have been shown to be markedly reduced or abolished by a dopamine antagonist. This effect of a dopamine antagonist was recently shown to be reversed by the glycine antagonist strychnine and by compounds that elevate intracellular cAMP levels. The present study was conducted to determine whether strychnine and cAMP-elevating compounds could bring out the surround ON responses in OFF-center ganglion cells that are diminished upon dark adaptation. Extracellular recordings of OFF-center brisk ganglion cells were made from isolated, superfused retinal preparations. During the course of dark adaptation, the surround On responses of many cells decreased markedly.Application in both brisk-transient and brisk-sustained OFF-center ganglion cells. The center OFF responses of these cells, on the other hand, were not enhanced by strychnine. Of the cAMP-elevating compounds tested, 8-(4-chlorophenylthio) cyclic AMP was the most effective in bringing out the surround ON responses in dark-adapted OFF-center ganglion cells. The findings from this study suggest that under dark-adapted conditions glycinergic neurons inhibit the surround component of OFF-center ganglion cells. The release of glycine from these neurons is suggested to be regulated by a cAMP-dependent mechanism.

The ultrastructural features and synaptic contacts of two amacrine cell types with corticotropin-releasing factor-like immunoreactivity in the turtle retina were examined using electron immunocytochemistry. Type A cells were found only in the visual streak and had elongated dendritic arborizations that ran parallel to the visual streak. These cells arborized primarily in stratum 1 and near the border of strata 2 and 3 of the inner plexiform layer, with some processes extending into stratum 5. Type B cells were found only ventral to the visual streak and arborized primarily in a wide band in strata 4 and 5, with sparse dendritic arborizations in stratum 1.

There was a diffuse cytoplasmic reaction product within each cell type; however, large labeled vesicles were rarely observed. Type A amacrine cells received many conventional synaptic contacts from amacrine cells in stratum 1 and at the border of strata 2 and 3, but only a small number of contacts in stratum 5. Bipolar synaptic contacts onto type A amacrine cells were observed in strata 1 and at the border of strata 2 and 3. The only positively identified synaptic outputs of type A cells were conventional synapses onto amacrine cells in strata 1 and at the border of 2 and 3. Type B amacrine cells received synaptic contacts from amacrine cells in strata 1 and 5, and bipolar cell synaptic input in stratum 5. They made conventional synapses onto amacrine cells in strata 1 and 5, and onto bipolar cells in stratum 5. We also found conventional synaptic contacts between unlabeled amacrine cells and type B amacrine cells outside of the primary layers of stratification. In addition, there were specialized junctions observed between type A cell profiles in stratum 1 and between type B cell profiles in stratum 5. The unique regional distributions of the type A and B cells, as well as their differences in synaptic connectivity, suggested that these amacrine cells play distinct physiological roles although they contain the same neuropeptide.

Larvae of the tobacco hornworm moth Manduca sexta were reared on either a carotenoid-supplemented or a carotenoid-deficient diet. The former yields fortified adults with normal visual function, whereas visual sensitivity and rhodopsin content are reduced by 2−4 log units in the compound eyes of the deprived moths reared on the latter. We characterized the retinoids of fortified retinas and investigated the recovery of visual function in deprived moths that were provided with retinaldehyde as a source of photopigment chromophore. Retinoids were identified and measured by high-performance liquid chromatography (HPLC). Fortified retinas contained mainly 3-hydroxyretinaldehyde (R3); 11-cis R3 predominated in dark-adaptation, all-trans in light-adaptation, indicating that R3 is the photopigment chromophore. No retinoids could be measured in deprived eyes. Retinaldehyde (R1) was delivered to the retinas of deprived moths by “painting” solutions of 11-cis or all-trans R1 in dimethylsulfoxide (DMSO) on the corneal surfaces of the compound eyes or on the head capsule between the eyes. 11-cis R1 induced rapid recovery: during 3 days, sensitivity rose to within a log unit of that measured from fortified animals. By 7 days, sensitivity was close to normal. Although rhodopsin and P-face particle densities of photoreceptor membranes increased, neither rose to the levels found in fortified animals. All-trans R1 induced only a slight increase in sensitivity that could have resulted from some nonspecific isomerization of the all-trans to the 11-cis isomer; we found no evidence for a retinal isomerase that functions in darkness. Small amounts of R3 were measured in recovering retinas, indicating some conversion of R1 to R3. However, the chromophore of most of the rhodopsin that was synthesized must have been R1. It is possible that rhodopsin did not reach normal levels in the retina even after a week of recovery because the normal chromophore R3 was not provided. Although the rhodopsin that initially formed in recovering moths may have resulted from the association of the chromophore with pre-existing opsin, the extent of eventual recovery indicates that opsin synthesis was stimulated by 11-cis R1.

Retinal ganglion cells within the same region of the retina may have different lengths of axon before reaching the optic disc depending on the route they take with respect to the temporal raphe. We have investigated whether there is a correlation between soma and intraretinal axon diameter and how these parameters relate to intraretinal axon length on both sides of the cat temporal raphe. Retinas were wholemounted and alpha-cell somata and fibers stained with a modified neurofibrillar method. Moving peripherally from the area centralis along the raphe there was a progressively increasing difference between the intraretinal axon lengths for nearly adjacent cells across the raphe, which reached a maximum of 4–5 mm at the retinal periphery. Cells on the nasal aspect of the raphe had shorter axons than did adjacent cells on the temporal aspect of the raphe. Comparison of soma diameter s&les across the raphe showed there was no clear trend between soma diameter and intraretinal length. Replotting the raphe and s&le areas on a cell density map indicated that différences in soma diameter could be attributed to ganglion-cell density differences between the s&led areas.

Examination of the stained cells revealed that within the initial length of the axon there was a region showing a reduction of axon diameter (diameter <1 μm), which varied in length from cell to cell. The axon was, therefore, divided into three segments: the portion of axon prior to thinning (A), the thin segment itself (B), and the part of the axon after the thin segment (C). The diameter of each segment (A, B, C) and the lengths of the first and second segments (A, B) were significantly correlated with soma diameter (P < 0.001). From measurements of the axon diameter of segment C, it was concluded that alpha-cell axons continue to increase in diameter along their path towards the optic disc.

The present report indicates that alpha-cell soma size, when going from the area centralis to the periphery along the raphe, reaches a plateau and then declines within more peripheral retinal locations in spite of increasing intraretinal axon length. Thus, there is no positive correlation between soma or axon diameter and intraretinal axon length. The anatomical findings are discussed in relation to previous reports of retinal development and complementary conduction times within intraretinal and extraretinal visual pathways.

Behavioral and electrophysiological methods were used to measure sensitivity to flickering lights in a dichromatic species, the California ground squirrel (Spermophilus beecheyi). Discrimination tests were used to determine spectral sensitivity at stimulus frequencies from 5–50 Hz and increment threshold spectral sensitivity. The contributions of retinal mechanisms to these capacities were assessed by recording the responses of optic nerve fibers to temporally modulated monochromatic lights. In the ground squirrel, as in the human, the shape of the spectral-sensitivity function depends on the temporal frequency of the stimulus. Results from single-unit recording show that all of the classes of optic nerve fibers in the ground squirrel are highly phase-locked to the stimulus for modulation rates as high as 50 Hz. Neither the responses of photoreceptors nor any class of optic nerve fiber can singly account for the behavioral results. The electrophysiological results are also counter to models which propose that temporally dependent changes in the spectral sensitivity of spectrally opponent fibers account for the behavior. The temporal resolution of the optic nerve fibers exceeds that of the behaving animal suggesting that retinal mechanisms do not limit behavioral temporal resolution.

The visual response to a flash given in the dark is known to saturate according to the Michaelis-Menten relationship. Nevertheless, the incremental response from increasing levels of mean luminance tends to follow a Weber-Fechner relationship well into the saturation range determined from the Michaelis-Menten results. This sensitivity transformation from Michaelis-Menten to Weber-Fechner is an important characteristic of light adaptation in the vertebrate retina. Recent studies concerning the role of calcium in photoreceptor adaptation have shown that the relaxation from peak to plateau in the response of isolated photoreceptors was absent under conditions in which adaptation was blocked. Comparing the pronounced relaxation from peak to plateau in turtle horizontal cells with the absence of such relaxation in the catfish response, we noted also that turtle incremental sensitivity shows a Weber-Fechner relationship while catfish incremental sensitivity more closely follows the local slope of the Michaelis-Menten relation. Based on these observations, we have obtained an expression to relate the relaxation from peak to plateau with the sensitivity transformation. We assume that adaptation shifts the half-maximum point of the Michaelis-Menten curve so that the light response relaxes to a plateau value equal to a specified fraction φ of the peak response. We show that this manipulation alone results in a transformation from Michaelis-Menten kinetics to Weber-Fechner sensitivity.

Intracellular recordings were made from rods in the superfused retina of the marine toad (Bufo marinus). It was found that injection of a brief depolarizing current pulse (0.04–1 nA) evoked a distinctive, long-lasting response, here called “the prolonged depolarization.” The response appears to be regenerative, has a stereotypical waveform, is typically about 6 mV in &litude and 3 s in duration, and has a relatively long recovery period (10–60 s). As a rule, the response cannot be directly evoked by light but the current-evoked response is significantly enhanced in the presence of steady illumination. The light-evoked hyperpolarization and the depolarizing spikes of the rod are both attenuated in the presence of the prolonged depolarization. The prolonged depolarization is not an altered manifestation of the depolarizing spikes of toad rods since both can be recorded simultaneously and steady illumination suppresses the spikes while enhancing the prolonged depolarization. The response is enhanced in chloride-free superfusate and also appears to be enhanced by the use of electrodes containing chloride. The response is markedly shortened in superfusates that lack calcium or contain 1–5 mM cobalt. On this and other evidence, it is suggested that the response may be generated by the sequential action of calcium channels and calcium-activated chloride channels. Although rarely evoked by light, the prolonged depolarization of toad rods is otherwise remarkably similar to the prolonged depolarization of turtle cones. It is proposed that the prolonged depolarization, in contrast to the feedback depolarization of cones, arises from mechanisms common to both rods and cones.

Immunocytochemical methods with antiserum to the calcium-binding protein parvalbumin (PV) were used to examine the effects of monocular enucleation on parvalbuminergic neurons and processes in the lateral geniculate nucleus (LGN) of adult rhesus monkeys. In the LGN of normal monkeys, numerous PV-positive neurons, including the largest neurons in the nucleus, and many PV-positive processes occur in all six laminae. After monocular enucleation, PV immunoreactivity is reduced in the neuropil of the denervated laminae compared to adjacent nondenervated and to normal laminae. PV immunoreactivity of somata in denervated laminae, however, appears to be indistinguishable from that of somata in nondenervated laminae, although neurons in the denervated laminae are smaller in size. Since LGN neurons in denervated laminae have lost their visual input, the functional role of PV in this nucleus may not relate directly to visual information processing.

Much attention has been paid to the effect of various types of neonatally induced retinal insults on neurons of the cat lateral geniculate nucleus (LGN). Little is known about cellular adjustment to functional altertions commencing in the adult. The present study was aimed at examining the effect of monocular enucleation or retinal impulse blockade on mature neurons of the cat LGN and perigeniculate nucleus. In addition to labeling the relay neurons with cytochrome oxidase (CO) histochemistry and immunohistochemistry, and presumed interneurons with GABA immunohistochemistry, the two markers were also combined in the same section. The results showed that GABA-immunoreactive neurons in the LGN can be subdivided into two major groups: highly immunoreactive neurons (Hir) and moderately immunoreactive neurons (Mir). These two groups differed slightly in their size and CO levels. With monocular enucleation or TTX treatment, there was a reduction in the numerical density of Hir and a concomitant increase in Mir in the affected laminae. However, there was no evidence of a reduction in GABA immunoreactivity in neurons of the perigeniculate nucleus. With regard to relay cells our data were in agreement with our previous findings (Kageyama & Wong-Riley, 1985) that there was a statistically significant positive correlation between cell size and CO levels, so that neurons with large cross-sectional areas were predominately darkly reactive for CO (Dco), while medium-to-small neurons were mainly moderate to lightly reactive (M/Lco). After monocular enucleation or TTX injections, the numerical density and size of Dco were significantly reduced, while those of M/Lco were proportionally increased in the affected laminae, indicating a conversion of some Dco to M/Lco. The results indicate that the maintenance of CO levels in predominately the large relay cells and GABA levels in a subclass of small neurons of the mature cat LGN are activity-dependent and are highly sensitive to retinal insults.

Direction-selective responses were recorded from neurons in the dorsal terminal nucleus (DTN) of the cat accessory optic system before and after intravitreal injections of tetrodotoxin (TTX) into the contralateral eye. After approximately 100 min, direction-selective responses driven through stimulation of the contralateral, injected eye were reduced on average by 90%, while direction-selective responses driven through stimulation of the ipsilateral, uninjected eye were not significantly reduced. By 200 min postinjection, ipsilateral direction-selective responses were either equal to or sometimes greater than control values. In the final stages of these experiments (i.e. between 390–830 min after contralateral eye injections), ipsilateral eye responses were on average 30% higher than control. The effects of retinal blockade of the contralateral eye by TTX show that input from the ipsilateral eye alone is sufficient to mediate direction-selective responses in DTN cells. These results and those observed following bicuculline eye injections reported previously (Grasse et al. 1990) demonstrate that direction-selective responses in the DTN driven through stimulation of the contralateral and ipsilateral eyes arise from independent neural mechanisms located in the retina and visual cortex, respectively. Moreover, these findings also suggest that the contralateral eye exerts an inhibitory influence over ipsilateral eye responses which is diminished by TTX injections into the contralateral eye.