During normal vision, when subjects attempt to fix their gaze on a small stimulus feature, small fixational eye movements persist. We have recorded the impulse activity of single neurons in primary visual cortex (V1) of macaque monkeys while their fixational eye movements moved the receptive-field activating region (AR) over and around a stationary stimulus. Three types of eye movement activation were found. (1) Saccade cells discharged when a fixational saccade moved the AR onto the stimulus, off the stimulus, or across the stimulus. (2) Position/drift cells discharged during the intersaccadic (drift) intervals and were not activated by saccades that swept the AR across the stimulus without remaining on it. To activate these neurons, it was essential that the AR be placed on the stimulus and many of these cells were selective for the sign of contrast. They had smaller ARs than the other cell types. (3) Mixed cells fired bursts of activity immediately following saccades and continued to fire at a lower rate during intersaccadic intervals. The tendency of each neuron to fire transient bursts or sustained trains of impulses following saccades was strongly correlated with the transiency of its response to stationary flashed stimuli. For one monkey, an extraretinal influence accompanying fixational saccades was identified. During natural viewing, the different eye movement classes probably make different contributions to visual processing. Position/drift neurons are well suited for coding spatial details of the visual scene because of their small AR size and their selectivity for sign of contrast and retinal position. However, saccade neurons transmit information that is ambiguous with respect to the spatial details of the retinal image because they are activated whether the AR lands on a stimulus contour, or the AR leaves or crosses the contour and lands in another location. Saccade neurons may be involved in constructing a stable world in spite of incessant retinal image motion, as well as in suppressing potentially confusing input associated with saccades.

The a-wave of the human dark-adapted ERG is thought to derive from activity of rod photoreceptors. However, other sources within the retina could potentially perturb this simple equation. We investigated the extent to which the short-latency dark-adapted rod a-wave of the primate ERG is dominated by the rod photoresponse and the applicability of the phototransduction model to fit the rod a-wave. Dark-adapted Ganzfeld ERGs were elicited over a 5-log-unit intensity range using short bright xenon flashes, and the light-adapted cone responses were subtracted to isolate the rod ERG a-wave. Intravitreal 4-phosphono-butyric acid (APB) and cis-2,3-piperidine-dicarboxylic acid (PDA) were applied to isolate the photoreceptor response. The Hood and Birch version of the phototransduction model, Rmax[1 − e−I·S·(t−teff)2] , was fitted to the a-wave data while allowing Rmax and S to vary. Three principle observations were made: (1) At flash intensities ≥0.77 log sc-td-s the leading edge of the normalized rod ERG a-wave tracks the isolated photoreceptor response across the first 20 ms or up to the point of b-wave intrusion. The rod ERG a-wave was essentially identical to the isolated receptor response for all intensities that produce peak responses within 14 ms after the flash. (2) The best fit of sensitivity (S) was not affected by APB and/or PDA, suggesting that the inner retina contributes very little to the dark-adapted a-wave. (3) APB always reduced the maximum dark-adapted a-wave amplitude (by 15–30%), and PDA always increased it (by 7–15%). Using the phototransduction model, both events can be interpreted as a scaling of the photoreceptor dark current. This suggests that activity of postreceptor cells somehow influences the rod dark current, possibly by feedback through horizontal cells (although currently not demonstrated for the rod system), or by altering the ionic concentrations near the photoreceptors, or by neuromodulator effects mediated by dopamine or melatonin.

Rod and cone photoreceptors send their signals to ON- and OFF-retinal ganglion cells through different pathways in the primate retina. We hypothesized that increments and decrements of light may be processed differently by the rod-bipolar pathway because of the funneling of the rod signal through the rod bipolar cell. We tested this hypothesis using a psychophysical adaptation paradigm, which has provided evidence that photopic increments and decrements of light are processed by ON- and OFF-pathways in the human visual system. We had observers adapt to either a rapid-on or rapid-off sawtooth waveform, under both photopic and scotopic conditions. We then measured detection thresholds for one cycle of a rapid-on or rapid-off sawtooth stimulus. For photopic stimuli, sawtooth adaptation asymmetrically raised thresholds for test stimuli in a manner that depended on the polarity of the adaptation stimulus. For scotopic stimuli, thresholds were raised, but no significant selective adaptation effect was found. By repeating the photopic condition with sawtooth stimuli which had been filtered using an impulse response function derived for the rod system, we demonstrated that the lack of selective adaptation was not a consequence of the sluggish temporal response of the rod-bipolar pathway. We conclude instead that the reduced effectiveness of sawtooth adaptation is due to channeling of rod photoreceptor signals through the rod bipolar cell before reaching ON- and OFF-ganglion cells.

To determine how a progressive loss of photoreceptor cells and the concomitant loss of glutamatergic input to second-order neurons can affect inner-retinal signaling, glutamate receptor expression was analyzed in the Royal College of Surgeons (RCS) rat, an animal model of retinitis pigmentosa. Immunohistochemistry was performed on retinal sections of RCS rats and congenic controls between postnatal (P) day 3 and the aged adult (up to P350) using specific antibodies against N-methyl-D-aspartate (NMDA) subunits. All NMDA subunits (NR1, NR2A–2D) were expressed in control and dystrophic retinas at all ages, and distinct patterns of labeling were found in horizontal cells, subpopulations of amacrine cells and ganglion cells, as well as in the outer and inner plexiform layer (IPL). NR1 immunoreactivity in the inner plexiform layer of adult control retinas was concentrated in two distinct bands, indicating a synaptic localization of NMDA receptors in the OFF and ON signal pathways. In the RCS retina, these bands of NR1 immunoreactivity in the IPL were much weaker in animals older than P40. In parallel, NR2B immunoreactivity in the outer plexiform layer (OPL) of RCS rats was always reduced compared to controls and vanished between P40 and P120. The most striking alteration observed in the degenerating retina, however, was a strong expression of NR1 immunoreactivity in Müller cell processes in the inner retina which was not observed in control animals and which was present prior to any visible sign of photoreceptor degeneration. The results suggest functional changes in glutamatergic receptor signaling in the dystrophic retina and a possible involvement of Müller cells in early processes of this disease.

The goal of this study was to determine whether the jellyfish green fluorescent protein (GFP) could be used in transgenic mice to label and purify cone photoreceptors from the living retina. We created a transgene containing the 5′ regulatory sequence of the human red pigment gene (pR6.5 lacZ clone; kindly provided by J. Nathans & Y. Wang), fused to the GFP coding sequence. This transgene was used to generate seven lines of PCR-positive founders. Three of the lines had bright green fluorescent cone photoreceptors. The GFP fills the entire cell. Two mouse lines had only a few (∼10–100) fluorescent cells per retina, and one line (R6.85933) had many thousands. In the latter, double labeling of the cones with RITC-conjugated peanut agglutinin reveals that in the ventral retina a small proportion of the cones express GFP, while in the dorsal retina the majority do. Cells dissociated from the retinae of line R6.85933 continue to fluoresce and can be readily detected and enriched with flow cytometry. The signal provides a log unit of separation between the fluorescent cone soma and the remaining retinal cells. Roughly 3% of the cells are this fluorescent, and it is possible to purify up to 30,000 cells from one mouse. RT-PCR analysis of the mRNA from these isolated cells detects both the middle and short wavelength opsins with little if any contamination from rhodopsin.

A sinusoidal mask grating oriented orthogonally to and superimposed onto an optimally oriented base grating reduces a cortical neuron's response amplitude. The spatial selectivity of cross-orientation suppression (XOR) has been described, so for this paper we investigated the temporal properties of XOR. We recorded from single striate cortical neurons (n = 72) in anesthetized and paralyzed cats. After quantifying the spatial and temporal characteristics of each cell's excitatory response to a base grating, we measured the temporal-frequency tuning of XOR by systematically varying the temporal frequency of a mask grating placed at a null orientation outside of the cell's excitatory orientation domain. The average preferred temporal frequency of the excitatory response of the neurons in our sample was 3.8 (± 1.5 S.D.) Hz. The average cutoff frequency for the sample was 16.3 (± 1.7) Hz. The average preferred temporal frequency (7.0 ± 2.6 Hz) and cutoff frequency (20.4 ± 6.9 Hz) of the XOR were significantly higher. The differences averaged 1.1 (± 0.6) octaves for the peaks and 0.3 (± 0.4) octaves for the cutoffs. The XOR mechanism's preference for high temporal frequencies suggests a possible extrastriate origin for the effect and could help explain the low-pass temporal-frequency response profile displayed by most striate cortical neurons.

The second messenger systems involved in the final stages of the phototransduction cascade in Limulus photoreceptors remain unclear. Excised patches of transducing membrane contain cGMP-gated channels, suggesting the involvement of cGMP in the excitation process. To further explore this possibility, we tested the effects of inhibitors and agonists of guanylate cyclase. The active site cyclase inhibitors guanosine 5′-tetraphosphate and adenosine 5′-tetraphosphate produced a reversible reduction of the response to light without affecting resting membrane properties. The cyclase inhibitor Rp-GTPαS produced a similar reduction, but the effect was only slightly reversible. The reduction in the response produced by these inhibitors was robust, often producing over a 95% decrease in the amplitude of the light response. Previous work had shown that an end-product cyclase inhibitor, imidodiphosphate, also inhibited the response. The consistent results with four different guanylate cyclase inhibitors strongly support the involvement of this enzyme in the phototransduction cascade. To determine whether the guanylate cyclase involved is the NO-dependent soluble form, we applied inhibitors and activators of the nitric oxide synthase/guanylate cyclase pathway such as L-N5-(1-iminoethyl) ornithine, sodium nitroprusside, and carboxy-PTIO. None of these agents had any substantial effect on phototransduction. Taken together, these results support a role for a particulate guanylate cyclase in Limulus photoreceptor excitation.

Recent studies imaging nitric oxide (NO) production in the retina have indicated a much wider distribution of NO production than would be suggested by previous light-microscopic localizations of neuronal nitric oxide synthase (nNOS). To help resolve this discrepancy, the present study analyzed the ultrastructural localization of nNOS-like immunoreactivity (-LI) in all layers of the retina. In the ellipsoids of rod photoreceptors and the accessory elements of double cones, nNOS-LI was associated with some atypical mitochondria. In the outer plexiform layer, nNOS-LI was in some postsynaptic horizontal and bipolar cell processes at photoreceptor ribbon synapses. In some amacrine and ganglion cell somata, nNOS-LI was diffusely localized in the cytoplasm and associated with the endoplasmic reticulum. In the inner plexiform layer, nNOS-LI diffusely filled some amacrine cell processes, while in other amacrine cells nNOS-LI was selectively localized at the presynaptic specializations of conventional synapses. Neuronal NOS-LI was also found at membrane specializations in bipolar cell terminals that were distinct from their normal ribbon synapses. Finally, some nNOS-LI was found in mitochondria in Müller cells. The diverse subcellular localizations of nNOS-LI indicates that NO may play distinct functional roles in many retinal cells, which correlates well with the widespread NO production found in previous NO imaging studies.

Previous work suggests that photoreceptor synaptic ribbon length and absolute dark-adapted threshold may vary during a 24-h diurnal cycle. To test this hypothesis, we examined the length of photoreceptor synaptic ribbons and the dark-adapted threshold in black (+/+) and albino (c2J/c2J) C57BL/6J mice at six times over a 24-h period. Testing began 2 h after light onset (ZT 2:00) and continued at successive 4-h intervals (12 h:12 h light:dark). We determined the length of the synaptic ribbons in frozen sections by labeling them with an antibody specific for synaptic ribbons. Synaptic ribbons vary in length at different points in the diurnal cycle in both types of mice, but the synaptic ribbons in black mice are longer than those in albino mice by an average of 0.33 μm. The synaptic ribbons of black mice also have a larger response to changes in the light cycle. Ribbon length in black mice ranges from 1.66 μm to 1.4 μm, whereas ribbon length in albino mice ranges from 1.32 μm to 1.25 μm. The shortest ribbons are evident 6 h after light onset in both types of mice, whereas the longest ribbons appear within 2 h after light onset. These changes in synaptic ribbon length support the idea that photoreceptor synaptic ribbons are dynamic structures whose length changes over a 24-h diurnal cycle. Examining black and albino mice with a water-maze behavioral assay showed that visual thresholds in black and albino mice vary over the 24-h diurnal cycle. The visual thresholds of albino mice are elevated compared with black mice at all times tested. This is consistent with previous findings of visual thresholds in hypopigmented mice. The lowest threshold (greatest sensitivity) is present 2 h after light onset (ZT 2:00) and corresponds to the time when synaptic ribbons are the longest. The highest threshold is observed 6 h after light onset, the time when synaptic ribbons are shortest. These results show that synaptic ribbon length and visual sensitivity vary together in relation to the time.

A preparation of isolated presynaptic terminals of rat retinal rod bipolar cells was developed. Patch-clamp recordings were performed on the isolated terminal to determine the type(s) of voltage-activated Ca2+ channels and the contribution of GABAA and GABAC receptor-mediated currents localized in the terminal region. Both low-voltage-activated (LVA) and high-voltage-activated (HVA) Ca2+ currents, with properties similar to those found in intact cell recordings, were observed in the isolated terminal recordings. Consistent with previous studies, the HVA Ca2+ currents are L-type since the currents were blocked by low micromolar concentrations of nimodipine and potentiated by BayK 8644. Also, both GABAA and GABAC receptor-mediated currents were observed in the isolated terminal. The current density of GABAC receptors in the terminal was more than three times higher than that in the soma. In contrast, the current density of GABAA currents between the terminal and the soma was not significantly different. Assessed by 100 μM GABA, the contributions of GABAA and GABAC receptors to the total GABA-mediated currents at the terminal were comparable. This study directly demonstrates the localization of LVA Ca2+ channels at the axon terminal of mammalian rod bipolar cells, suggesting that LVA Ca2+ channels may play a role in bipolar cell transmitter release. Results of this study also support the notion that both types of ionotropic GABA receptors regulate synaptic transmission in mammalian rod bipolar cells. In addition, this study reports for the first time the feasibility of direct patch-clamp recordings of isolated axon terminals of mammalian retinal bipolar cells. The isolated presynaptic terminal preparation of mammalian retinal bipolar cells could be a valuable system for the study of transmitter release in the central nervous system (CNS).

It is widely accepted that human color vision is based on two types of cone-opponent mechanism, one differencing L and M cone types (loosely termed “red–green”), and the other differencing S with the L and M cones (loosely termed “blue–yellow”). The traditional view of the early processing of human color vision suggests that each of these cone-opponent mechanisms respond in a bipolar fashion to signal two opponent colors (red vs. green, blue vs. yellow). An alternative possibility is that each cone-opponent response, as well as the luminance response, is rectified, so producing separable signals for each pole (red, green, blue, yellow, light, and dark). In this study, we use psychophysical noise masking to determine whether the rectified model applies to detection by the postreceptoral mechanisms. We measured the contrast-detection thresholds of six test stimuli (red, green, blue, yellow, light, and dark), corresponding to the two poles of each of the three postreceptoral mechanisms. For each test, we determined whether noise presented to the cross pole had the same masking effect as noise presented to the same pole (e.g. comparing masking of luminance increments by luminance decrement noise (cross pole) and luminance increment noise (same pole)). To avoid stimulus cancellation, the test and mask were presented asynchronously in a “sandwich” arrangement (mask-test-mask). For the six test stimuli, we observed that noise masks presented to the cross pole did not raise the detection thresholds of the test, whereas noise presented to the same pole produced a substantial masking. This result suggests that each color signal (red, green, blue, and yellow) and luminance signal (light and dark) is subserved by a separable mechanism. We suggest that the cone-opponent and luminance mechanisms have similar physiological bases, since a functional separation of the processing of cone increments and cone decrements could underlie both the separation of the luminance system into ON and OFF pathways as well as the splitting of the cone-opponent mechanisms into separable color poles.

Gamma-aminobutyric acid (GABA) is the most prevalent inhibitory neurotransmitter in the vertebrate brain. It can exert its influence either as GABAergic projection pathways or as local interneurons, which play an essential role in many visual functions. However, no GABAergic visual pathways have been studied in frogs so far. In the present study, GABAergic pathways in the central visual system of Rana pipiens were investigated with double-labeling techniques, combining immunocytochemistry for GABA with Rhodamine microspheres for retrograde tracing. Three GABAergic visual pathways were identified: (1) a retino-tectal projection, from retina to the contralateral optic tectum (OT); (2) an ipsilateral projection from the nucleus of the basal optic root (nBOR) to the pretectal nucleus lentiformis mesencephali (nLM); and (3) a second-order pathway from the nucleus isthmi (NI), bilaterally, to the optic tectum. These results indicate that GABA is involved in both first-order (retina to optic tectum) as well as second-order (nucleus isthmi to optic tectum) visual projections in Rana pipiens, and may play a major role in mediating visuomotor reflexs such as optokinetic nystagmus or other visually guided behaviors.

Pseudorabies virus (PRV) has been shown to be an effective transneuronal tracer within both the peripheral and the central nervous system. The only investigations of this virus in the visual system have examined anterograde transport of PRV from injection sites in the retina. In the present study, we injected attenuated forms of PRV into the primary visual cortex of both rats and cats to determine whether transneuronal retrograde infection would occur back to the retina. In rats, we made small injections into visual cortex of a strain of PRV (Bartha Blu) that contained a β-galactosidase promoter insert. In cats, we injected PRV-M201 into area V1 of visual cortex. After a 2- to 4-day incubation period, we examined tissue from these animals for the presence of the β-galactosidase marker (rats) or the virus itself (cats). Cortical PRV injections resulted in transneuronal retrograde infection of the lateral geniculate nucleus (LGN), thalamic reticular nucleus (TRN), and retina. PRV was retinotopically distributed in the pathway. In addition, double-labeling experiments in cats using an antibody against gamma-aminobutyric acid (GABA) were conducted to reveal PRV-labeled interneurons within the LGN and TRN. All TRN neurons were GABA+, as was a subset of LGN neurons. Only the subset of TRN neurons adjacent to the PRV-labeled sector of LGN was labeled with PRV. In addition, a subset of GABA+ interneurons in LGN was also labeled with PRV. We processed some tissue for electron microscopy to examine the morphology of the virus at various replication stages. No mature virions were detected in terminals from efferent pathways, although forms consistent with retrograde infection were encountered. We conclude that the PRV strains we have used produce a local infection that progresses primarily in the retrograde direction in the central visual pathways. The infection is transneuronal and viral replication maintains the intensity of the label throughout the chain of connected neurons, providing a means of examining detailed circuitry within the visual pathway.

The mosaics of S-cones and the neurons to which they are connected are relatively well characterized, so the S-cone system is a good vehicle for exploring how the sampling of the retinal image controls visual performance. We used an interferometer to measure the grating acuity of the S-cone system in the fovea and at a range of eccentricities out to 20 deg. We also developed a simple model observer that, by assuming only that cone pathways are noisy and that signals are subject to eccentricity-dependent postreceptoral pooling, predicts the measured acuities from the sampling properties of the S-cone mosaic. The amount of pooling required to explain performance is consistent with that suggested by anatomical and physiological measurements.

The vertebrate retina contains only five major neuronal classes but these embrace a great diversity of discrete types, many of them hard to define by classical methods. Consideration of their spatial distributions (mosaics) has allowed new types, including large ganglion cells, to be resolved across a wide range of vertebrates. However, one category of large ganglion cells has seemed refractory to mosaic analysis: those that project to the accessory optic system (AOS) and serve vestibulocerebellar mechanisms of motion detection and image stabilization. Whenever AOS-projecting cells have been analyzed by nearest-neighbor methods, their distribution has appeared almost random. This is puzzling, because most aspects of visual processing require the visual scene to be sampled regularly. Here, spatial correlogram methods are applied to distributions of large ganglion cells, labeled retrogradely from the AOS in frogs, turtles, and rats, and to the AOS-projecting displaced ganglion cells of chickens. These methods reveal hidden spatial order among AOS-projecting populations, of a form that can be simulated either by superimposing a single regular mosaic on a random population or, more interestingly, by overlapping three or more regular, similar but spatially independent mosaics. The rabbit is known to have direction-selective ganglion cells (not, however, AOS projecting) that can be subdivided into functionally distinct, regular mosaics by their tracer-coupling patterns even though they are morphologically homogeneous. The present results imply that the direction-selective AOS-projecting ganglion cells of all vertebrates may, likewise, be subdivided into regular, independent mosaics.

We have previously reported that a small number of retinal ganglion cells (RGCs) of adult cats survive 2 months after transection of the optic nerve (ON) and that α cells have the greatest ability to survive among different types of RGCs (Watanabe et al., 1995). Here we report the time course of RGC survival within 15 days after ON transection using retrograde labeling with DiI injected into the bilateral lateral geniculate nuclei of cats. The density of DiI-labeled RGCs in the central retina as well as in the periphery did not change until day 3 after ON transection, then decreased rapidly, to 43% of the original density on day 7, and falling to 19% by day 14. We then intracellularly injected Lucifer yellow into the DiI-labeled RGCs to examine the difference in the time course between surviving α and β cells. Similar to the density change in total surviving RGCs, the proportion of surviving β cells did not change until day 3, then decreased rapidly to 65% of the original density on day 4, falling to 12% by day 14. By contrast, 64% of α cells survived for 14 days after axotomy. Analysis of regression lines for survival time courses indicated that death of β cells was characterized with a rapid period phase from day 3 to day 7 after axotomy whereas that of α cells lacked it. Axon-like sprouting from surviving β cells was first recognized in the nerve fiber layer on day 3, and were later more conspicuous.

The voltage-gated calcium and sodium currents of starburst amacrine cells were examined in slices of the adult rabbit retina. ON-center starburst amacrine cells were targeted for whole-cell recording by prelabeling the retina with the nuclear dye 4′-6-diamidino-2-phenylindole hydrochloride (DAPI). Calcium currents were isolated using an external Ringer that contained tetrodotoxin to block sodium currents and barium to block potassium channels. When starburst amacrine cells were stepped to holding potentials positive to −50 mV, a series of voltage-dependent calcium currents were activated. The calcium current peaked at −10 mV. The calcium currents kinetics were mainly sustained in nature, showing only a small amount of slow inactivation. Nickel (100 μM), a T-type channel blocker, had no effect on the calcium current. Application of the L-type channel agonist BAY K8644 (1–2.5 μM) had small variable effects on the calcium current while the L-type channel antagonist nifedipine (10 μM) had no effect. However, addition of a reported N-type calcium channel antagonist, omega-conotoxin G6A (1 μM), blocked a large portion of the calcium current, as did a more nonselective antagonist, omega-conotoxin M7C (200 nM). Agatoxin 4A (500 nM) reduced a smaller sustained calcium current component, implying a P/Q-type calcium channel was present on these neurons. In addition to the calcium currents, a fast voltage-gated sodium current was observed in many starburst cells. This current could be blocked by tetrodotoxin (200–500 nM). The differing kinetics and durations of the sodium and calcium currents could play important roles in the regulation of synaptic release and in the coordination of spiking by starburst amacrine cell dendrites during retinal development and in the encoding of motion across the retinal surface.

Spatial and temporal properties related to direction selectivity of both simple and complex type visual cortex neurons were assessed by cross-correlation analysis of their responses to random ternary white noise. This stimulus consisted of multiple randomly placed bars, each colored white, black, or gray with equal probability, which were rerandomized every 5–10 ms. A first-order cross-correlation analysis of a neuron's spike train with the spatiotemporal history of the stimulus provided an estimate of the neuron's linear spatiotemporal filtering properties. A nonlinear correlation analysis measured the amount of interaction for pair-wise combinations of bars as a function of their relative spatial and temporal separations. The spatiotemporal orientation of each of these functions was quantified using a “motion energy index” (MEI), which was compared to the neurons' direction selectivity measured with drifting sinewave gratings. Both first-order and nonlinear correlation plots usually showed s–t orientation whose sign was consistent with the neuron's direction preference; however, in many cases the MEI for first-order analysis was weak compared to that seen in the nonlinear interactions. The structures of the nonlinear interaction functions were also compared with predictions from a conventional model of direction selectivity based on a simple spatiotemporally oriented linear filter, followed by an intensive nonlinearity (“LN model”). These comparisons showed that some neurons' data agreed reasonably well with such a model, while others agreed poorly or not at all. Simulations of an alternative model which combines signals from idealized lagged and nonlagged front-end linear filters produce noise correlation results more like those seen in the neurophysiological data.

The neuronal generators of the b- and d-waves of the electroretinogram (ERG) were investigated in the tiger salamander retina to determine if amacrine and ganglion cells contribute to this field potential. Several agents were used that affect third-order neurons, such as tetrodotoxin, baclofen, and NMDA agonists and antagonists. Baclofen, an agent that enhances light responses in third-order neurons, increased the d-wave and reduced the b-wave. In contrast, agents that decrease light responses in third-order neurons had the opposite effect of enhancing the b-wave and depressing the d-wave. The effect on the d-wave was particularly pronounced. The results indicate that third-order neuronal activity influences b- and d-waves of the ERG. The opposing actions suggest that the b-wave to d-wave ratio might serve as an measure of ganglion cell function.

The purpose of the present study was to compare and contrast behavioral performance on three different tasks of spatial cognition during unilateral and bilateral reversible deactivation of posterior parietal cortex. Specifically, we examined posterior middle suprasylvian (pMS) sulcal cortex in adult cats during temporary and reversible cooling deactivation. In Task 1, the cats oriented to a high-contrast, black visual stimulus moved into the visual field periphery. In Task 2, the cats oriented to a static light-emitting diode (LED). Task 3 examined the cats' ability to determine whether a black-and-white checkered, landmark box was closer to the right or left side of the testing apparatus. Following training on all tasks, cryoloops were implanted bilaterally within the pMS sulcus. Unilateral deactivation of pMS sulcal cortex resulted in virtually no responses to either moved or static stimuli and virtually no responses to landmarks presented in the contralateral hemifield, and a profound contralateral hemifield neglect was induced. Responses to stimuli and landmarks presented in the ipsilateral hemifield were unimpaired. Additive, bilateral cooling of the homotopic region in the contralateral hemisphere, but not an adjacent region, resulted in reversal of the initial hemineglect for the moved stimulus, yet induced a complete failure to orient to peripheral static LED stimuli. Bilateral cooling also reversed the contralateral neglect of the landmark, but then cats could not accurately determine position of the landmark anywhere in the visual field because performance was reduced to chance levels for all landmark loci in both hemifields. In this instance, as the contralateral neglect disappeared during bilateral cooling of pMS cortex, a new spatial discrimination deficit was revealed across the entire visual field. We conclude that pMS cortex contributes in multiple ways to the analyses of space, and that these contributions cannot be safely predicted from analyses of unilateral deactivations or from one task to another. Moreover, it is clear that other structures are capable of guiding orienting to high contrast, moved targets when pMS cortex is eliminated from brain circuitry. However, these same structures are incapable of supporting either orienting to static stimuli or analyses of spatial relations as tested with the landmark task. The impact of reversible deactivation of the superior colliculus on these same tasks is discussed.