In the fish retina, retinomotor movement, spinule formation, and alteration of connexon density within gap junctions occur in response to changes in ambient light conditions. All of these morphological parameters can also be influenced by the application of dopamine. This study examines whether the morphological alterations of these structures are correlated with the activity of endogenous dopamine during an entrained 12-h light/12-h dark cycle and after 1-h sort-term adaptation periods.

The two measured parameters of retinomotor movement, cone inner segment length and pigment dispersion, were well-correlated with endogenous cyclic dopamine activity. However, retinomotor movement was initiated already at the end of the entrained dark period, before the onset of light and before the onset of dopamine turnover. Furthermore, a 1-h dark-adaptation period in the middle of the light phase reduced dopamine activity but did not affect retinomotor movement. At the switch from light to dark and after a 1-h light period at midnight retinomotor movement correlated exactly with dopamine turnover and illumination conditions. The formation of spinules was correlated with dopaminergic activity during all phases of the light/dark cycle and during short-term adaptation periods. Spinules were expressed in the light when dopamine activity was high and they were retracted when dopamine activity was reduced during darkness. Connexon density of horizontal cell gap junctions showed a weaker correlation with the endogenous dopamine turnover. In this case, a high activity of endogenous dopamine was paralleled by a high density of connexons.

Our results suggest that endogenous dopamine is involved in the cyclic regulation of the observed morphological alterations and that dopamine is part of the light signal for these mechanisms.

We examined a white-eyed strain of the norpA mutant (norpA;cn bw) and white (w)norpA+ controls using microspectrophotometry (MSP), electron microscopy (EM), and electroretinography (ERG). These studies revealed that light mediates receptor demise in norpA even though norpA lacks phototransduction. Rhodopsin and the rhabdomere which houses it decrease with increasing age in norpA but not in w with rearing on a 12 h light/12-h dark cycle or in constant light. At higher temperature in norpA;cn bw and w reared in constant light, visual pigment decreases, rhabdomeres diminish, and cells die. Importantly, dark rearing blocked visual pigment loss in norpA;cn bw; the M-potential, an ERG reflection of visual pigment level, corroborated this finding. MSP showed that norpA's visual pigment loss was not due to acute loss of metarhodopsin, rhodopsin's photoproduct. NorpA blocks certain processes expected to be light elicited. The alteration of visual pigment as a function of time of day, present in w controls, is absent in white-eyed norpA, suggesting that light-induced depolarization may be necessary to entrain the rhythm. Microspectrofluorometry using the fluorescent dye, Lucifer yellow, suggested that norpA lacks a light-induced uptake mechanism; using control flies, we determined the stimulus parameters required for uptake in vivo. An attempt to “cure” norpA;cn bw by replacement “therapy” using phospholipase C, missing in norpA's phototransduction cascade, was largely unsuccessful.

Specific antisera, raised in rabbits, against somatostatin 1-14, somatostatin 1-28, the fragment 1-12 of somatostatin 1-28, and prosomatostatin 20-36 were used for immunohistochemistry and gel filtration of the rat retina.

With all antisera, immunoreactive perikarya could be located in the inner nuclear and ganglion cell layers. In the inner nuclear layer, amacrine cells with processes extending predominantly into the first sublayer of the inner plexiform layer were observed. Some processes extended also to the ganglion cell layer. In addition, somatostatin-immunoreactive interplexiform cells were present in the inner nuclear layer.

In the ganglion cell layer, perikarya were found located in the midperiphery and in the far periphery of the retina. The neurons located in the midperiphery of the retina possessed a round perikaryon from which processes could be followed going into the inner plexiform layer, where they dichotomized in the third and first sublayers. The perikarya in the far periphery of the retina near the ora serrata exhibited an ovoid-shaped cell body from which processes extended horizontally in a bipolar manner in the layer itself.

By use of an [35S]-labeled antisense oligonucleotide probe, in situ hybridization of the rat retina showed the presence of perikarya in the inner nuclear layer and ganglion cell layer containing mRNA encoding for prosomatostatin.

Gel filtration of the retinal extracts followed by radioimmunoassay showed the presence of somatostatin 1-14, the fragment 1-12 of somatostatin 1-28, and prosomatostatin 1-64. However, somatostatin 1-28 was not detected.

The results obtained in this study verify the presence of somatostatin 1-14 in the rat retina located in perikarya and processes in the inner nuclear and ganglion cell layers. The positive in-situ hybridization signals show that the intraneuronal somatostatin immunoreactivity is due to synthesis of the peptide and not uptake in the neurons. The presence of the somatostatin propeptide and fragments of this propeptide, in both intraretinal perikarya and fibers, indicate a posttranslational modification of this neuropeptide in the perikarya and the processes as well.

The receptive-field profile of the cone in cat retina was computed. The computation was based on (1) the known anatomical circuit connecting cones via narrow-field bipolar cells to the on-beta ganglion cell; (2) the known physiological receptive-field profile of the on-beta (X) cell at the corresponding eccentricity; and (3) a model in which the beta receptive field arises by linear superposition of cone receptive fields. The computed cone receptive field has a center/surround organization with a center almost as broad as that of the beta cell center. The cone surround is comparably broad to that of the beta cell but somewhat lower in peak amplitude. The problems to which the center/surround receptive field are the solution, namely, signal compression and noise reduction, apparently must be solved before the first synapse of the visual pathway.

We studied quantitatively the receptive-field properties of 74 units recorded from the representation of the central visual fields in the cat's lateral suprasylvian (LS) visual cortex. In agreement with previous workers, we found that LS receptive fields tended to be large and to lack discernible spatial structure. They resembled the complex receptive fields of areas 17 and 18 in their general organization. We examined the responses of these neurons to moving optimally oriented sinusoidal gratings that varied in spatial and temporal frequency of drift. Most LS neurons were selective for the spatial frequency of sinusoidal gratings; 7% responded to all spatial frequencies below a cutoff value. In agreement with previous reports, the optimal spatial frequencies for LS neurons covered a wider range than is seen in either area 17 or 18 alone (0.05–1 cycle/deg), but are certainly included in the range covered by both these afferent areas. Individual neurons in LS responded to a range of spatial frequencies broader than is typical for neurons in areas 17 and 18. The effect of varying the drift rate of otherwise optimal gratings was similar in LS to that reported for areas 17 and 18. Most neurons were optimally responsive to drift rates between 0.5 and 4 Hz, and resolved frequencies as high as 10–30 Hz. A few neurons had optima higher than 6 Hz and resolved frequencies in excess of 30 Hz. We conclude that the receptive fields of LS neurons reflect rather closely the properties of their afferents from areas 17 and 18. Apart from the increased incidence of directional selectivity in LS and the increase in receptive-field size seen there, we find no evidence for a significant reorganization of visual signals.

The role of GABA in the outer plexiform layer of the turtle retina has been examined by intracellular recordings from L- and C-type horizontal cells in the isolated retina preparation.

GABA (1–5 mM) slightly depolarized the L-type horizontal cells, reduced the amplitude of their photoresponses, and slowed down the rate of hyperpolarization during the ON component of the photoresponse. These effects could not be replicated by either muscimol or baclofen. When synaptic transmission from the photoreceptors had been blocked by either kynurenic acid or cobalt ions, GABA depolarized L-type horizontal cells and augmented the remaining photoresponses. Neither muscimol nor baclofen exerted any effect on L-type horizontal cells under these conditions. Nipecotic acid, a competitive inhibitor of the GABA-uptake system, induced effects on turtle L-type horizontal cells which were similar to those exerted by GABA. Thus, the complex GABA effect on turtle L-type horizontal cells seems to represent the summation of at least two actions; an indirect one mediated by the red cones via GABAa-type receptors and a direct one which probably reflects the activation of an electrogenic GABA-uptake system.

GABA (1–5 mM) induced a transient depolarization in C-type horizontal cells but eliminated color opponency in only three cells out of seven studied. This observation is inconsistent with the notion that the only neural mechanism responsible for the chromatic properties of C-type horizontal cells in the turtle retina is a GABAergic negative feedback from the L-type horizontal cells onto the green ones.

Postsynaptic responses of tectal cells in the bullfrog (Rana catesbeiana) were intracellularly recorded following electrical stimulation of the optic tract and the nucleus isthmi, and fluorescent dye, Lucifer yellow, was injected into some of the impaled cells to show their morphologies. Two main response types were found: The first type was an EPSP followed by an IPSP, and the second type was single IPSP. The first type predominates in cells responding to the optic tract stimulation and the second type prevails in cells responding to the isthmic stimulation. Fifteen cells stained with Lucifer yellow were localized in layer 6 (11 cells), layer 7 (1 cell), and layer 8 (3 cells). They were mainly identified as pear-shaped cells, large ganglionic cells, and stellate cells. Three injections demonstrated “dye-coupling,” which labeled up to six cells following one injection. Comparisons of postsynaptic potentials with cellular morphologies suggested that the nucleus isthmi could directly excite large ganglionic neurons in layer 6. Synaptic mechanisms for strong isthmic inhibition on the tectal neurons remain unknown.

Previous electrophysiological studies have shown that neurons in the nucleus of the basal optic root (nBOR) of the pigeon respond best to wholefield stimuli moving slowly in a particular direction in the contralateral visual field. In this study, we have found that some nBOR neurons respond to wholefield stimulation of both eyes. These binocular neurons have spatially separate receptive fields in both visual fields. Some binocular neurons prefer the same direction of wholefield motion in both eyes, and thus respond best to wholefield visual motion which would result from translation movements of the bird, either ascent, descent, or forward and backward motion. Other neurons prefer opposite directions of wholefield motion in each eye and therefore respond optimally to wholefield visual motion simulating rotational movements of the bird, either roll or yaw. These binocular neurons may play a crucial part in the locomotor behavior of the pigeon by providing visual information distinguishing translational and rotational movements.

The presence and concentrations of each of the three subtypes of opioid receptors (mu, kappa, and delta) has been studied in the accessory optic nuclei (dorsal, lateral, and medial terminal nuclei and the interstitial nucleus of the superior fasciculus, posterior fibers: DTN, LTN, MTN, and inSFp) in normal young rats with radioligands directed towards each opioid receptor subtype. The changes in mu opioid receptors have also been investigated in monocularly enucleated rats in which one eye was removed and the rats sacrificed at postoperative day (PO) 2, 3, 5, 7, 14, and 30. As the MTN is the only accessory optic nucleus of the rat large enough for semiquantitative evaluation, the mu receptor population of the MTN has been subjected to optical microdensitometric analysis.

All four of the accessory optic nuclei (AOS nuclei) are found to contain exceedingly high levels of mu opioid receptor binding with the selective radioligand [3H]-[D-Ala, MePhe4, Gly-ol5] (DAGO), low levels of kappa opioid receptor binding using the radioligand [3H]-[ethylketocyclazocine] (EKC) together with the competing agents [D-Pro4]-morphiceptin and [D-Ser2, Thr6]-Leu-enkephalin, and an absence of delta opioid receptor binding with the radioligand [3H]-[D-A1a2, D-Leu5]-enkephalin (DADLE) combined with the competing agent [D-Pro4]-morphiceptin. Monocular enucleation, as studied on the mu opioid receptor population with this experimental approach, results in virtually a complete loss of mu opioid receptors throughout all four of the contralaterally located AOS nuclei, including both dorsal and ventral subdivisions of the medial terminal nucleus (MTNd, v). Kappa and delta receptors are very few (kappa receptors) or are lacking (delta receptors) in the AOS nuclei, and for this reason, the effects of monocular enucleation on these two opioid receptor subtypes have not been investigated. Monocular enucleation also produces a significant lowering in mu receptor binding in other primary optic nuclei (the lateral geniculate nuclei, nucleus of the optic tract, and superficial layers of the superior colliculus) and in the pars principalis of the medial geniculate nucleus (description of changes in mu receptors in non-accessory optic primary optic nuclei will be considered elsewhere).

Microdensitometric study of the MTNd, v shows that the decreased binding of mu receptors in this nucleus is barely detectable (about 6%) at PO2 and rises to 6–15% at PO3. At PO5 receptor loss reaches approximately 62%, whereas at PO7 it is about 81% complete. At PO14 and PO30, the mu receptor loss is nearly complete at around 93%. Mu receptor loss involves all of the AOS nuclei contralateral, but none ipsilateral, to ocular enucleation, an observation entirely consistent with the overwhelmingly crossed (about 97%) nature of the retinofugal projection to the rat accessory optic nuclei. These opioid receptors represent a prominent feature in the AOS and other primary optic nuclei of the rat. Their role in visuomotor control remains uncertain but probably involves the fine-tuning of information concerned with compensatory eye movements.