The validity of the Barten theoretical model for describing the vertebrate spatial contrast sensitivity function (CSF) and acuity at scotopic light levels has been examined. Although this model (which has its basis in signal modulation transfer theory) can successfully describe vertebrate CSF, and its relation to underlying visual neurophysiology at photopic light levels, significant discrepancies between theory and experimental data have been found at scotopic levels. It is shown that in order to describe scotopic CSF, the theory must be modified to account for important mechanistic changes, which occur as cone vision switches to rod vision. These changes are divided into photon management factors [changes in optical performance (for a dilated pupil), quantum efficiency, receptor sampling] and neural factors (changes in spatial integration area, neural noise, and lateral inhibition in the retina). Predictions of both scotopic CSF and acuity obtained from the modified theory were found to be in good agreement with experimental values obtained from the human, macaque, cat, and owl monkey. The last two species have rod densities particularly suited for scotopic conditions.

Tyrosine hydroxylase (TH) expression was used as a marker to study the dopaminergic cells in the Cebus monkey retina. Two types of dopaminergic cells were identified by cell body size and location, level of arborization in the inner plexiform layer, and amount of immunolabeling. Type 1 cells displayed intense immunoreactivity and larger somata (12–24 μm) located in the inner nuclear layer or ganglion cell layer, whereas type 2 had smaller cell bodies (8–14 μm) found either in the inner plexiform layer or ganglion cell layer and were more faintly labeled. Interplexiform cells were characterized as type 1 dopaminergic cells. Immunoreactive axon-like processes were seen in the nerve fiber layer, and a net of fibers was visible in the foveal pit and in the extreme periphery of the retina. The population of TH+ cells was most numerous in the temporal superior quadrant and its density peaked at 1–2 mm from the fovea. Type 1 TH+ cells were more numerous than type 2 cells at any eccentricity. Along the horizontal meridian, type 1 cell density was slightly higher in temporal (29 cells/mm2) than in nasal (25 cells/mm2) retina, while type 2 cells had a homogeneous distribution (4.5 cells/mm2). Along the vertical meridian, type 1 cells reached lower peak density (average 17.7 cells/mm2) in the inferior retina (central 4 mm), compared to the superior portion (23.7 cells/mm2). Type 2 cell density varied from 4.5 cells/mm2 in the superior region to 9.4 cells/mm2 in the inferior region. The spatial density of the two cell types varied approximately inversely while the total density of TH+ cells was virtually constant across the retina. No correlation between dopaminergic cells and rod distribution was found. However, we suggest that dopaminergic cells could have a role in mesopic and/or photopic vision in this species, since TH+ fibers are present in cone-dominated regions like the foveola and extreme nasal Periphery.

The distribution of glycinergic synapses in macaque monkey retina was investigated. The monoclonal antibody (mAb2b) against the αl subunit of the glycine receptor produced a punctate immunoreactivity that was localized to synapses. In central retina about 70% of the αl subunit-containing synapses were located in strata 1 and 2 of the inner plexiform layer, about 30% were located in strata 3 and 4, and immunoreactivity was absent in stratum 5. Electron microscopy showed that the majority of the synapses in strata 1 and 2 were on cone bipolar axons. The presynaptic profile always belonged to an amacrine cell. Presynaptic and postsynaptic profiles were further characterized using double-label immunofluorescence with cell-type specific antibodies against calcium-binding proteins. An antiserum against calretinin was used to label A<doubt/>II amacrine cells and an antiserum against recoverin was used to label flat midget bipolar cells. In the outer part of the IPL, 75% of the αl-immunoreactive puncta were colocalized with calretinin-immunoreactive An processes and 61% of the αl-immunoreactive puncta were colocalized with recoverin-positive midget bipolar axons. These results suggest that the αl subunit of the glycine receptor is present at the chemical synapse made by A<doubt/>II amacrine cells with flat midget bipolar cells, thus providing a pathway for rod signals to reach midget ganglion cells.

In the human rod visual system, self-cancellation of flicker signals is observed at high rod intensity levels near 15 Hz, both perceptually and in the electroretinogram (ERG). This and other evidence suggests that two rod signals are transmitted through the human retina with different speeds of transmission. Here we report a series of flicker ERG recordings from a normal observer and an observer who lacks cone vision. From these results, we propose a quantitative model of the two rod signals, which assumes (1) that the amplitude of the slow signal grows linearly with log intensity but then saturates at ~1 scot, td; (2) that the amplitude of the fast signal grows linearly with intensity; (3) that there is a difference in time delay of ~33 ms between two rod signals of the same polarity (or of ~67 ms if the signals are of inverted polarity); and (4) that the time delay of both signals declines linearly with log intensity (by ~10 ms per log scot. td). These simple assumptions provide a remarkably good account of the experimental data. Our results and model are relevant to current anatomical theories of the mammalian rod visual system. We speculate that the slower signal in the human ERG may reflect the transmission of the rod response via the rod bipolars and the An amacrine cells, while the faster signal may reflect its transmission via the rod-cone gap junctions and the cone bipolars. There are, however, several objections to this simple correspondence.