Light causes a rapid, 1.7-fold increase in cyclic GMP concentration in intact squid retinas (Johnson et al. (1986)). To determine whether light-induced changes in cyclic GMP concentration result from activation of guanylate cyclase, we have studied the regulation of guanylate cyclase activity in squid (Loligo pealei) photoreceptors. The enzyme is membrane-associated and activity is enhanced by the detergents Triton X-100 or digitonin. The enzyme requires divalent cations, Mn2+ being preferred over Mg2+. The dependence of enzyme activity on the MnGTP concentration deviates from simple Michaelis-Menten kinetics. Under conditions where a light-induced binding of GTP to the guanine nucleotide regulatory protein can be observed, no light-induced change in guanylate cyclase could be detected.

γ-aminobutyric acid (GABA) has been reported to be an important neurotransmitter in the retinas of many species. This immunocytochemical study detailed the localization of antigens resembling GABA and glutamic acid decarboxylase (GAD, an enzyme involved in the synthesis of GABA), in retinal neurons in the turtle, Pseudemys scripta elegans. GABA-like immunoreactivity was present within somata in the inner and outer regions of the inner nuclear layer, within somata in the ganglion cell layer, and in processes in the outer plexiform layer, inner plexiform layer, and ganglion cell axon layer. GAD-like immunoreactivity was found in somata in the inner and outer regions of the inner nuclear layer and in processes in the inner and outer plexiform layers. Cell counts indicated more somata with GABA-like than GAD-like immunoreactivity in the inner nuclear layer. Double-label studies showed that every somata in the inner nuclear layer which had GAD-like immunoreactivity also had GABA-like immunoreactivity, but that many somata had only GABA-like immunoreactivity.

The stratification of immunoreactivity within the inner plexiform layer was analyzed using a scanning densitometer. We described the strata within the inner plexiform layer such that S0 represented the inner nuclear layer/inner plexiform layer border and S100 represented the inner plexiform layer/ganglion cell layer border. Analysis of GAD-like labeling yielded seven distinct strata with peak densities at positions S8, S19, S28, S42, S59, S75, and S93. GABA-like labeling provided five distinct strata with peak densities at positions S17, S28, S67, S84, and S95. The strata with peaks of GABA-like immunoreactivity at S17 and S28 were in statistically identical locations to corresponding strata with GAD-like immunoreactivity. The strata with GABA-like immunoreactivity at S67, S84, and S95 did not have statistically identical peaks of correlated GAD-like immunoreactivity, although there were corresponding strata with GAD-like immunoreactivity nearby. Antiserum directed against GABA failed to produce labeled strata at positions corresponding to the strata with GAD-like immunoreactivity at S8 and S42.

In summary, our results indicated that the antisera we used, which were directed against GABA and GAD, produced significantly different labeling in the inner nuclear layer, inner plexiform layer, and the ganglion cell body and axon layers of the turtle retina. Until the physiological significance of these differences is resolved, studies employing these markers to investigate the function of GABA in the turtle retina should be interpreted with caution.

The development of synaptic ribbons in rod and cone photoreceptor terminals of the cat retina was studied using quantitative electron microscopy. At the region of the area centralis, synaptic ribbon profiles are initially recognized at PCD (postconception day) 59. Synaptic ribbon density increases rapidly, reaching a peak of 0.55 ribbons/μm3 at PCD 68 (postnatal day 3) and maintains approximately that value for an additional 8 d. Following PCD 76, ribbon density begins to decrease, to 0.37 ribbons/μm3 at PCD 82 and 0.25 ribbons/μm3 at PCD 102. Although ribbon density drops by approximately 50% during this 39-d period, the outer plexiform layer (OPL) volume at the area centralis increases by about 20%. Ribbon density continues to decrease gradually over a protracted period to reach a final adult value of 0.11–0.14 ribbons/μm3. During the period of high ribbon density, rod spherules with two, or even three ribbon profiles, were routinely observed. In contrast, in the adult, spherules with more than one ribbon profile are only rarely encountered. During development, the length of synaptic ribbon profiles increases from a mean of 0.22 μm at PCD 62 to the 0.47 μm mean length found in the adult.

Light dependence of the effects of taurine depletion on retinal function and biochemistry was examined in albino rats housed either in cyclic lighting or in continuous darkness. Measurements of retinal taurine, DNA, and rhodopsin contents, and electroretinogram amplitudes were made at weekly intervals. Naka-Rushton parameters were estimated for the b wave amplitude-intensity function. No significant effects of lighting regime were observed on retinal taurine levels in untreated rats, or on the time course or extent of taurine depletion in animals treated with guanidinoethyl sulfonate, an antagonist of taurine transport. In both lighting schemes, treatment led to a linear reduction of retinal taurine content which plateaued after 5–6 weeks at 50% of control despite continued treatment. DNA values did not differ among groups, whereas rhodopsin levels doubled in both groups of dark-maintained rats. For treated rats housed in cyclic lighting, the onset of electroretinogram deficits paralleled the loss of retinal taurine in the absence of changes in rhodopsin levels or cell death. Vmax was significantly reduced after 4 weeks of treatment. In contrast, for rats housed in continuous darkness, there were no significant differences in electroretinogram parameters between control and taurine-depleted rats until after 10–14 weeks of treatment. This implies that light exposure accelerates the appearance of functional changes associated with retinal taurine deficiency. The basis of the light dependence and the interpretation of related studies is discussed.

Rod and cone photoresponses in a variety of species have been accurately described with linear multistage filter models. In this study, the response latency and initial coding of intensity at two higher levels of visual processing are related to such photoreceptor responses. One level is the retinal output (spiking discharges from frog ganglion cells, based on experimental data reported here), the other is the perceptual level in humans (psychophysical latency and brightness functions, based on data from the literature). Photoreceptor responses are described with the “independent activation” model of Baylor et al. (1974). The intensity dependence of the early ganglion cell discharge, its latency and initial impulse frequency, is shown to follow from such a waveform, assuming that 1) latency L = l + D, where l is the time it takes for the rod response linearly summed over the ganglion cell's receptive field to reach a criterion amplitude, and D is a constant delay; and 2) the initial frequency (below saturation) is proportional to the steepness of rise of the summed rod response at time l. It is shown that the intensity dependences of 1) human visual latency and 2) brightness sensation, including effects of stimulus area and duration, are accounted for by the same model. The predicted functions are not power functions of intensity, but approximate such over wide ranges. Thus, a large body of psychophysical data is explained simply by the waveform of photoreceptor responses.

The projections of the nucleus of the optic tract were studied in the cat by simultaneous use of two distinct retrograde tracers (Fast Blue and Diamidino Yellow) injected in the inferior olive and the prepositus hypoglossi nucleus. Following injections of diamidino yellow in one structure and fast blue in the other, a significant number of retrogradely labeled neurons projecting to either target were observed dispersed in the nucleus of the optic tract. Three populations of labeled cells were found: one which projected to the inferior olive, a second to the nucleus prepositus hypoglossi, and a third which projected by means of a bifurcating axon to both of these structures. Quantification of these results reveals that 72% of the total number of labeled neurons are labeled by the IO injection, the remaining cells being labeled by the NPH injection. Double-labeled neurons represent more than 7% of the total number of the labeled cells. Tentative inferences as to the electrophysiological properties of the nucleus of the optic tract are discussed in the context of the optokinetic system.

In this study, we have investigated the organization of mouse visual cortex by correlating in detail the distribution of striate-extrastriate projections with the pattern of callosal connections revealed by the transport of horseradish peroxidase from the contralateral hemisphere. Single injections of 3H-proline into striate cortex produce 8–9 discrete projection fields in the belt of cortex surrounding area 17. The number and arrangement of these fields closely resemble the pattern of extrastriate visual areas in the rat. The callosal pattern is also very similar to that in the rat, and provides a set of landmarks for the location of the striate-recipient zones. Thus, cortical regions containing dense aggregations of callosal cells and terminations surround totally or partially the sparsely callosal striate-recipient zones. By comparing our results with previous accounts of the rat visual plan, we were able to identify in lateral extrastriate cortex of the mouse areas anterolateral (AL), lateromedial (LM), laterointermediate (LI), laterolateral (LL), posterolateral (PL), and posterior (P). We also observed 1–2 projections fields into anteromedial (AM) extrastriate cortex, and one field (S) into the posteromedial border of the head representation in primary somatosensory cortex. Our results support the notions that the visual cortex in the mouse is subdivided into multiple visual areas, and that these areas are arranged according to a plan that is common in rodents.

A photon-counting retinal densitometer is described that has been designed optically and electronically for improved sensitivity and reliability. The device allows measurement of visual pigments through the undilated natural pupils of subjects at relatively low levels of measuring lights, and serves also as an adaptometer for direct comparisons between pigment bleaching or regeneration and light or dark adaptation. Instrumental control and data collection are by computer to permit rapid and simple data analysis and comparisons between subjects. The methods by which the sensitivity and reliability have been enhanced are described in detail, and some examples of experimental results are presented.