Nitric oxide (NO) is a novel neuronal messenger that likely influences retinal function by activating retinal guanylyl cyclase to increase levels of cGMP. In the present study, the localization of neuronal nitric oxide synthase (nNOS, Type I NOS) in the cone-dominant tree shrew retina was studied using NADPH-d histochemistry and nNOS immunocytochemistry. Both NADPH-d and nNOS-immunoreactivity (IR) labeled the inner segments of rods and the myoids of a regular subpopulation of cones, with their corresponding nuclei outlined. The labeled cone myoids were co-localized with a marker for short-wave-sensitive (SWS) cones (S-antigen) and also displayed the regular triangular packing and density (7%) characteristic of SWS cones in tree shrew and other mammalian retinas. These measures confirmed the identity of the labeled cones as SWS cones. Photoreceptor ellipsoids of all cones were strongly labeled by NADPH-d reactivity, but lacked nNOS-IR. Another novel finding in tree shrew retina was that both NADPH-d and nNOS-IR labeled Müller cells, which have not been labeled by nNOS-IR in other mammalian retinas. Consistent with findings in rod-dominant retinas, two types of amacrine cells at the vitreal edge of the inner nuclear layer and a subpopulation of displaced amacrine cells at the scleral edge of the ganglion cell layer were labeled by both NADPH-d and nNOS-IR. Processes of these labeled cells were seen to extend into the inner plexiform layer, where dense punctate label was seen, especially in the central sublamina. These results show that localization of NOS in the cone-dominant tree shrew retina shares some common properties with rod-dominant mammalian retinas, but also shows some species-specific characteristics. The new finding of nNOS localization in tree shrew SWS cones and rods, but not in other cones, raises interesting questions about the roles of NO in the earliest level of visual processing.

The thalamus is the major gate to the cortex and its control over cortical responses is well established. Cortical feedback to the thalamus is, in turn, the anatomically dominant input to relay cells, yet its influence on thalamic processing has been difficult to interpret. For an understanding of complex sensory processing, detailed concepts of the corticothalamic interplay need yet to be established. Drawing on various physiological and anatomical data, we elaborate the novel hypothesis that the visual cortex controls the spatiotemporal structure of cortical receptive fields via feedback to the lateral geniculate nucleus. Furthermore, we present and analyze a model of corticogeniculate loops that implements this control, and exhibit its ability of object segmentation by statistical motion analysis in the visual field.

The synaptic organization of GABA-immunoreactive (GABA-IR) amacrine cells in the inner plexiform layer (IPL) of salamander retina was studied with the use of postembedding immuno-electron microscopy. A total of 457 GABA-IR amacrine synapses, with identified postsynaptic elements, were analyzed on photomontages of electron micrographs covering 3,618 μm2 of the IPL. GABA-IR amacrine synapses were distributed throughout the IPL, with a small peak at the proximal margin of sublamina a. The majority of the output targets (81%) were GABA(−) neurons. Most of the contacts were simple synapses with one postsynaptic element identified as a process of an amacrine cell (55%), bipolar cell (19%) or ganglion cell (26%), and serial synapses were very rare. Of the 89 postsynaptic bipolar terminals, 63% participated in a reciprocal feedback synapse with the same presynaptic GABA-IR amacrine profile. There appeared to be no preference between GABA-IR amacrine contacts with rod- or cone-dominated bipolar cells (9.1% vs. 8.9%) or in the total number of amacrine synapses in sublaminas a and b (52% vs. 47%). The preponderance of amacrine cell input to bipolar cells in the OFF layer was derived from GABA-IR cells. These findings provide ultrastructural support to the existing physiological studies regarding the functional roles of the GABAergic amacrine cells in this species. Our results have added to the data base demonstrating that, in contrast to mammals, GABA-IR amacrine cells in amphibians and other nonmammals contact other amacrine cells more frequently, suggesting greater involvement of GABAergic amacrine cells in modulating lateral inhibitory pathways.

When intense adapting lights are turned off, the pupil of the turtle, Pseudemys scripta elegans, enlarges. The recovery functions for pupillary dilation have different time constants that are defined by red- and green-sensitive cones and rods as they are affected by prior light adaptation and time in the dark. Pupillary area related to dilation responds over at least a three- to four-fold range. Following white-light adaptation, the course of pupil dilation in the dark shows a three-legged curve of differing time constants. With spectral-light adaptations, the contributions of separate classes of photoreceptors can be isolated. Red- and green-sensitive cones contribute shorter time constants of 3.31 and 3.65 min to prior white-light adaptation—4.81 and 4.18 min to prior spectral-light adaptations. Rods contribute a much longer time constant of 6.69 min to prior white-light adaptation—7.60 min to prior spectral-light adaptation. The ratios are in keeping with the flash sensitivities of photoreceptors in this same animal, as well as with psychophysical visual threshold mechanisms of color sensitivity.

Behavioral and electrophysiological measures were used to elucidate the retinal modulation of oculomotor control in the turtle. Eye movements were recorded following intravitreal applications of 2-amino-4-phosphonobutyrate (APB) and the GABA antagonists picrotoxin and bicuculline. Visual responses of single basal optic nucleus (BON) neurons of the accessory optic system were studied in parallel experiments. The effectiveness of APB, a glutamate analog thought to act selectively on the retinal ON pathway, was assessed independently by recording electroretinograms or ganglion cell activity.

Injections of APB into the turtle's eye reduced or blocked the injected eye's ability to drive horizontal optokinetic nystagmus, as also observed in rabbit and cat (Knapp et al., 1988; Yucel et al., 1989). Single-unit recordings from the BON during APB superfusion (50–200 μM APB) of the contralateral retina demonstrated that these cells, which are direction-sensitive and respond to the offset of light flashes, have their responses to moving stimuli blocked by APB.

During the APB effect, GABA antagonists were applied to the same eye. Although moderate doses of APB were sufficient to block optokinetic or BON light responses, the addition of GABA blockers still elicited a spontaneous temporal-to-nasal nystagmus (Ariel, 1989) or visually responsive yet direction-insensitive responses from BON cells (Schuerger et al., 1990). These results are discussed in terms of the retinal output to pathways involved in oculomotor control of optokinetic nystagmus.

The effects of vasoactive intestinal peptide (VIP) on the extracellularly recorded activity of ganglion cells were studied in superfused rabbit retinas. VIP, applied to the bathing solution, significantly increased the maintained activity of both OFF-center and ON-center brisk ganglion cells. The transient, excitatory responses of these cells to flashes of light (spots or annuli centered over the receptive field) were either unaffected or moderately reduced. VIP did not affect the responses of most ON/OFF directionally selective ganglion cells to a moving light stimulus. Furthermore, maintained activity of most of these cells remained absent.

Effects of VIP on the light responses of ganglion cells were pronounced in retinas that were bathed with the dopamine D1 antagonist (+)-SCH 23390. For OFF-center brisk ganglion cells, VIP brought out both the center and surround excitatory responses that were selectively reduced by (+)-SCH 23390. Similarly, VIP brought out the leading edge responses that were reduced by (+)-SCH 23390 in ON/OFF directionally selective ganglion cells to a moving light stimulus. VIP did not however reverse the effects of (+)-SCH 23390 on ON-center brisk ganglion cells. It is argued that VIP counteracts the effects of (+)-SCH 23390 on OFF-center brisk ganglion cells and ON/OFF directionally selective ganglion cells by stimulating adenylate cyclase activity in dopamine-receptive cells of the retina.

Immunocytochemistry was used to study the distribution of gamma-aminobutyric acid (GABA) throughout the central visual nuclei and retina in Rana pipiens. In the retina, GABA immunoreactivity (both somata and fibers) was observed in all layers except the outer nuclear layer (ONL). Contrary to earlier reports, about 30% of total neurons within ganglion cell layer (GCL) expressed GABA immunoreactivity. Double-labeling studies indicated that about half of the GABA-containing perikarya in the GCL were retinal ganglion cells (RGCs). In the diencephalon, intensely labeled GABA-immunoreactive neurons and nerve fibers were observed within the neuropil of Bellonci (nB) and corpus geniculatum (CG), while only immunoreactive puncta were found in the rostral visual nucleus (RVN). In the pretectal region, the posterior thalamic nucleus (nPT) contained the most intensely labeled GABA immunoreactive perikarya and nerve fibers in the entire brain. Lightly immunoreactive perikarya were also found in the large-celled nucleus lentiformis mesencephali (nLM), as well as in the pretectal gray, which contains neurons postsynaptic to the retinal terminal zones within nLM. In the optic tectum (OT), both immunoreactive perikarya and fibers were found within superficial layers 8 and 9, whereas only densely packed immunoreactive perikarya were evident in the deep tectal layers (i.e. 2, 4, 6). The nucleus of the basal optic root (nBOR) contained a small number of lightly labeled GABA-immunoreactive perikarya, mostly located in the dorsal half of the nucleus. A large number of perikarya within the nucleus isthmi (NI) were also immunostained.

The nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) signal transduction pathway plays a role in every retinal cell type. Previous studies have shown that excitatory glutamatergic synaptic pathways can increase cGMP-like immunoreactivity (cGMP-LI) in retina through stimulation of NO production, but little is known about the role of synaptic inhibition in the modulation of cGMP-LI. Gamma-amino-n-butyric acid (GABA) plays critical roles in modulating excitatory synaptic pathways in the retina. Therefore, we used GABA receptor antagonists to explore the role of GABAergic inhibitory synaptic pathways on the modulation of the NO/cGMP signal-transduction system. Cyclic GMP immunocytochemistry was used to investigate the effects of the GABA receptor antagonists bicuculline, picrotoxin, and (1,2,5,6-tetrahyropyridin-4-yl) methylphosphinic acid (TPMPA) on levels of cGMP-LI. Cyclic GMP-LI was strongly increased in response to the GABAA receptor antagonist bicuculline, while the GABAC receptor antagonist TPMPA had little effect on cGMP-LI. The GABAA/GABAC receptor antagonist, picrotoxin, caused a moderate increase in cGMP-LI, which was mimicked by the combination of bicuculline and TPMPA. The nitric oxide synthase inhibitor, S-methyl-L-thiocitrulline (SMTC), blocked the increased cGMP-LI in response to stimulation with either bicuculline or picrotoxin. Treatments with either of the glutamate receptor antagonists (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) partially blocked the increases in cGMP-LI seen in response to bicuculline, but a combination of MK-801 and CNQX completely eliminated these increases. These results suggest that inhibitory synaptic pathways involving both types of GABA receptors work through excitatory glutamatergic receptors to regulate the NO/cGMP signal-transduction pathway in retina.

Glycine- and GABA-activated currents were examined in the axon terminals of 12 types of rabbit cone bipolar cells. In the superfused retinal slice, a cell was voltage clamped at 0 mV in the presence of cobalt; then glycine or GABA was puffed onto the axon terminal. Types CBa1, CBa2, and a few CBa1-2 cells demonstrated larger glycine-activated currents than GABA-activated ones. However, some OFF cells (CBa2n, CBa1-2n, CBa1w), most CBa1-2, and most ON cells (CBb3, CBb3-4, CBb3n, and CBb4) displayed larger GABA-activated currents. The ON cell, CBb5, possessed only a GABA-activated current. The predominance of glycinergic currents in CBa1, CBa2, and a few CBa1-2 cells suggests a major input from the glycinergic AII amacrine cell and thus a key role for these cells in the rod bipolar pathway. Certain OFF cells (most CBa1-2) expressed larger GABA-activated currents. All types expressed both GABAA and GABAC currents about equally, although most OFF types (CBa1, CB a2n, CBa1-2, and CBa2n) displayed a slightly greater GABAA component.

Previous evidence concerning the physiological cell classes in the medial interlaminar nucleus (MIN) has been conflicting. We reexamined the MIN using standard functional tests to distinguish X-, Y- and W-cells. Discharge patterns to flashing spots also were used to identify some cells as lagged or nonlagged, as previously done for the geniculate A-layers. Also, each cell's response timing (latency and absolute phase) was measured from discharges to a spot undergoing sinusoidal luminance modulation. Of 71 MIN cells, 48% were Y, 27% were W, 8% were X, and 17% were unclassifiable. Lagged and nonlagged discharge profiles were observed in each cell group, with 28% of all cells being lagged. Lagged cells displayed a response suppression and long latency to discharge following spot onset, and a slow decay in firing at spot offset that was often preceded by a transient discharge. These profiles were indistinguishable from those of lagged cells in the A-layers. MIN cells also were heterogeneous in response timing, displaying a range of latency and absolute phase values similar to that in the A-layers. We extended these analyses to 27 cells in the geniculate C-layers. In layer C, 35% of cells were Y, 10% were X, 25% were W, and 30% were unclassifiable. About 11% had lagged profiles, and were X-cells or unclassifiable cells. Layers C1 and C2 contained only W-cells and no lagged profiles. The range of timings in the C-layers was somewhat narrower than in the MIN. Overall, these results show that the MIN contains a greater variety of functional cell classes than heretofore appreciated. Further, it appears that mechanisms which create different timing delays in the A-layers also exist in the MIN and layer C. These timings may contribute to direction selectivity in extrastriate cortex.

Ca2+-dependent synaptic transmission from retinal amacrine cells is thought to be initiated locally at dendritic processes. Hence, understanding the spatial and temporal impact of Ca2+ transport is fundamental to understanding how amacrine cells operate. Here, we provide the first examination of the local effects of mitochondrial Ca2+ transport in neuronal processes. By combining mitochondrial localization with measurements of cytosolic Ca2+, the local impacts of mitochondrial Ca2+ transport for two types of Ca2+ signals were investigated. Disruption of mitochondrial Ca2+ uptake with carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone (FCCP) produces cytosolic Ca2+ elevations. The amplitudes of these elevations decline with distance from mitochondria suggesting that they are related to mitochondrial Ca2+ transport. The time course of the FCCP-dependent Ca2+ elevations depend on the availability of ER Ca2+ and we provide evidence that Ca2+ is released primarily via nearby ryanodine receptors. These results indicate that interactions between the ER and mitochondria influence cytosolic Ca2+ in amacrine cell processes and cell bodies. We also demonstrate that the durations of glutamate-dependent Ca2+ elevations are dependent on their proximity to mitochondria in amacrine cell processes. Consistent with this observation, disruption of mitochondrial Ca2+ transport alters the duration of glutamate-dependent Ca2+ elevations near mitochondria but not at sites more than 10 μm away. These results indicate that mitochondria influence local Ca2+-dependent signaling in amacrine cell processes.

Immunocytochemical techniques have been used to examine the distribution of substance-P (SP)-labeled neurons in the superior colliculus of rats from birth to adulthood. At birth, there are almost no SP-immunopositive neurons in the tectum. A small number of SP neurons appear over the next several days. However, the vast majority of SP neurons appear between P9 and P10, and by P12 have attained adult-like numbers and distribution. Neurons are confined to the superficial layers of the colliculus, specifically the upper two-thirds of the stratum griseum superficiale (SGS). There is no indication of a differential developmental sequence along rostrocaudal or mediolateral axes. Neuronal types can be distinguished as early as P6 and include horizontal, vertical, and multipolar cells.

Substance-P-immunoreactive axons and boutons are also present in the superior colliculus at birth, and are for the most part confined to the deep layers. Boutons are generally of the en-passant type. The density of labeled axons and boutons increases progressively, and by P10 there is an almost adult-like lamination and patchiness. In the adult, labeled axons and boutons are most dense in the stratum opticum and stratum griseum intermedium. Bridges of dorsoventrally oriented labeled axons span the relatively label-poor stratum album intermedium. SP label in the stratum griseum profundum is dense and patchy, and there is also dense label in the stratum album profundum bordering the periaqueductal grey.

The role of substance-P-labeled neurons in the superior colliculus is still a matter of speculation. The findings of this study indicate that SP neurons may play a role in intrinsic collicular circuitry.

The early development of the optic tract in hamsters was studied by labeling retinal axons with Dil applied to the eye, and then examining the labeled axons in flatmount preparations of the rostral brain stem. This technique permits a panoramic view of the entire retinal projection, from the chiasm to the caudal end of the superior colliculus. In the Ell embryo, retinal axons have reached the chiasm. They defasciculate as they emerge from the nerve, prior to reaching the ventral midline of the diencephalon, then converge again as they pass over to the opposite side. At the midline, many axonal trajectories crisscross, implying some shuffling of relative positions. Retinal axons are tightly bundled within the optic tract. Upon reaching the ventral border of the lateral geniculate body (LGB), they splay out over the nucleus, revealing a wavefront of pioneer axons individually distributed across the rostro-caudal extent of the LGB. Later-emerging retinal axons course over the surface of the thalamus in waves; subsequent waves of axons interdigitate between the lead fibers without fasciculating along them. Past the LGB, the axons undergo a second change in relative positions as the ribbon of fibers swerves caudally, prior to entering the superior colliculus. Retinal axons are tipped with growth cones of varying morphologies. No strong correlation is evident between the Structural complexity of the growth cone and its position within the tract. In the majority of cases, ipsilaterally and contralaterally directed axons follow a similar developmental course along the optic tract, without any indication of a temporal lag in the ipsilateral projection as claimed in earlier reports. Understanding the changes in spatial distribution of embryonic retinal axons as they navigate along the optic tract provides a further step towards elucidating how point-to-point projections form in developing sensory systems.

We have described the currents flowing across the presynaptic membranes of the four median photoreceptors of the giant barnacle, Balanus nubilus, using a quasi-voltage clamp arrangement. Membrane potential, measured in the terminal region of one photoreceptor, was controlled in all four terminals by feedback current supplied through the nerve containing the photoreceptors’ axons. The [Ca2+] ∘ in the saline was reduced to decrease the Ca2+ current, enabling better voltage control, and tetraethylammonium ion (TEA, 20 mM) was added to block a fast voltage-dependent K+ conductance.

Depolarizing voltage steps from the resting potential in the dark (−60 mV) evoked slow, inward Ca2+-dependent currents which could be blocked by Co2+, Mg2+, or Cd2+. The Ca2+ currents were followed by large outward currents that persisted for many seconds after the offset of moderate or large pulses. These tail currents increased in magnitude and duration with pulse duration and reversed at about −80 mV, consistent with previous evidence for a Ca2+-activated K+ conductance in this membrane. When the Ca2+-activated outward current was reduced to zero by increasing the [K+]∘ so as to set EK at −20 mV, and then stepping the voltage to this value, the step evoked a steady inward Ca2+ current. Thus, the Ca2+ current did not show voltage- or Ca2+-dependent inactivation. When Ba2+ was substituted for Ca2+, 500-ms depolarizing steps evoked steady inward currents but no outward currents. In any given experiment, the activation voltage of the Ca2+ or Ba2+ current did not depend on holding potential.

At the barnacle photoreceptor’s synapse, the postsynaptic cell adapts to maintained presynaptic voltage by a mechanism that is not understood. We conclude that neither Ca2+ current inactivation nor a shift in activation voltage with holding potential can account for this adaptation.

Visual pigments from the red rods of adults of eight species of Australian anuran amphibians, from a variety of habitats, were analyzed by microspectrophotometry. The λmax in all cases fell between 502 nm and 506 nm, and the absorption spectra were well fitted by an A1-based visual pigment template curve. Red rod pigments were also analyzed for a number of tadpoles. In some cases the data were best fitted with an A1based visual pigment template, in other cases with an A2-based template, and finally some tadpoles appeared to have mixtures of the two pigments.

The present study tested the hypothesis that nondominant-eye influences on lateral geniculate nucleus (LGN) neurons affect the processing of spatial and contrast information from the dominant eye. To do this, we determined the effects of stimulating the nondominant eye at its optimal spatial frequency on the responses of LGN cells to sine-wave gratings of different spatial frequency and contrast presented to the dominant eye. Detailed testing was carried out on 49 cells that had statistically significant responses to stimulation of the nondominant eye alone.

Spatial-frequency response functions to nondominant-eye stimulation indicated that the responses were spatially tuned, as reported previously (Guido et al., 1989). Optimal spatial frequencies through the nondominant eye were significantly correlated with the optimal spatial frequencies through the dominant eye (r = 0.54; P < 0.0001), and the optimal spatial frequencies were fairly similar for the two eyes.

Nondominant-eye stimulation changed the maximal amplitude of the fundamental (Fl) response to dominant-eye stimulation for only about 45% (22 of 49) of the cells that responded to nondominant-eye stimulation alone. The response vs. contrast function through the dominant eye was altered for 73% of the cells (51% independent of spatial frequency). Three types of effects were observed: a change in the initial slope of the response vs. contrast function (contrast gain), a change in the response amplitude at which saturation occurred, or an overall change in response at all contrasts. The incidence of these changes was similar for X and Y cells in LGN layers A, Al, and C (only four W cells were tested).

Nondominant-eye stimulation had little or no effect on the sizes or sensitivities of the receptive-field centers or surrounds for the dominant eye. In addition, nondominant-eye stimulation had little or no effect on optimal spatial frequency, spatial resolution, or the bandwidth of spatial-frequency contrast sensitivity curves for the dominant eye.

Possible functions of binocular interactions in the LGN are considered. The present results suggest a role in interocular contrast-gain control. Interocular contrast differences can occur before the acquisition of binocular fusion, when the two eyes are viewing different aspects of a visual stimulus. Psychophysical and physiological studies suggest that an interocular mechanism exists to maintain relatively constant binocular interactions despite differences in interocular contrast. The present results suggest that at least part of this mechanism occurs in the LGN.

The cervico-ocular reflex (COR) was investigated in the chameleon. Two kinds of responses were observed by oscillating the body (sine-wave stimuli) in the fixed-head animal: a "smooth response" of very low gain (around 0.08) and a saccadic response composed of 1–12 saccades per cycle of stimulation (depending on the stimulation frequency). Both responses were elicited in the compensatory direction (same direction as the stimulation) and exhibited a frequency dependence with low-pass properties. The saccadic response was especially developed and displayed a higher gain (up to 0.4) than the smooth response. In darkness, the saccades were triggered near the zero point (head-body alignment), whereas in the presence of a fixed visual surround they were elicited more regularly throughout the stimulation cycle. The amplitude of saccades was increased in the light. Consequently, the gain and the phase lag of the saccadic reponse were enhanced by the visual input. No visuo-cervical interaction was observed for the smooth response. Oscillating the body at a constant velocity (seesaw or ramp stimuli) revealed a frequency effect on the number of saccades (during a cycle of stimulation), but not on the gain of the response. Increasing the amplitude of oscillations augmented only very slightly the amplitude of saccades and consequently decreased the gain. Hence, the best working range of the saccadic response corresponds to body or head movements of low amplitude (up to ±20 deg) and low frequency (up to 0.25 Hz), and is improved by a visual input. These properties are discussed on a comparative point of view. It is proposed that, in chameleons, the saccadic response could contribute to gaze stabilization and add to the vestibulo-ocular and the optokinetic responses.

It might be expected that normal trichromatic females would perform as well as normal trichromatic males of the same age when tested with standard clinical color-vision tests that use pseudoisochromatic vanishing designs on neutral gray backgrounds such as the Hardy-Rand-Rittler (HRR) pseudoisochromatic plates and the Neitz Test of Color Vision (NTCV). Here 2966 children aged 6–13 years from four municipalities in Norway were tested in their school classrooms with the NTCV. Children who made errors on the test were retested. 187 males and 152 females made one or more errors on retest, and each was tested individually on the Richmond HRR Fourth Edition. 8% of the males were defined as color deficient when a double criterion for failing was applied, that is, one or more errors on the NTCV and two or more errors on the HRR. The calculated frequency of color-deficient females (homozygotes) for the same criterion is 0.42%. By contrast, 3% of females failed the criterion that gave a stable population of color-deficient males. This result is considered in relation to reports of female carriers of color-vision deficiency having problems with the Ishihara test and of females having poorer color discrimination than males.

We discuss hypotheses that link the measurements we can make with infants to inferences about their developing neural mechanisms. First, we examine evidence from the sensitivity to visual stimulus properties seen in infants’ responses, using both electrophysiological measures (transient and steady-state recordings of visual evoked potentials/visual event-related potentials) and behavioral measures and compare this with the sensitivity of brain processes, known from data on mammalian neurophysiology and human neuroimaging. The evidence for multiple behavioral systems with different patterns of visual sensitivity is discussed. Second, we consider the analogies which can be made between infants’ behavior and that of adults with identified brain damage, and extend these links to hypothesize about the brain basis of visual deficits in infants and children with developmental disorders. Last, we consider how these lines of data might allow us to form “inverse linking hypotheses” about infants’ visual experience.

Early in development, before the onset of vision, the retina establishes direction-selective responses. During this time period, the retina spontaneously generates bursts of action potentials that propagate across its extent. The precise spatial and temporal properties of these “retinal waves” have been implicated in the formation of retinal projections to the brain. However, their role in the development of direction selective circuits within the retina has not yet been determined. We addressed this issue by combining multielectrode array and cell-attached recordings to examine mice that lack the CaV3.2 subunit of T-type Ca2+ channels (CaV3.2 KO) because these mice exhibit disrupted waves during the period that direction selective circuits are established. We found that the spontaneous activity of these mice displays wave-associated bursts of action potentials that are altered from that of control mice: the frequency of these bursts is significantly decreased and the firing rate within each burst is reduced. Moreover, the projection patterns of the retina demonstrate decreased eye-specific segregation in the dorsal lateral geniculate nucleus (dLGN). However, after eye-opening, the direction selective responses of CaV3.2 KO direction selective ganglion cells (DSGCs) are indistinguishable from those of wild-type DSGCs. Our data indicate that although the temporal properties of the action potential bursts associated with retinal waves are important for activity-dependent refining of retinal projections to central targets, they are not critical for establishing direction selectivity in the retina.