Increment threshold functions of the electroretinogram (ERG) b–wave were obtained from goldfish using an in vivo preparation to study intraretinal mechanisms underlying the increase in perceived brightness induced by depletion of retinal dopamine by 6–hydroxydopamine (6–OHDA). Goldfish received unilateral intraocular injections of 6–OHDA plus pargyline on successive days. Depletion of retinal dopamine was confirmed by the absence of tyrosine-hydroxylase immunoreactivity at 2 to 3 weeks postinjection as compared to sham-injected eyes from the same fish. There was no difference among normal, sham-injected or 6–OHDA-injected eyes with regard to ERG waveform, intensity-response functions or increment threshold functions. Dopamine-depleted eyes showed a Purkinje shift, that is, a transition from rod-to-cone dominated vision with increasing levels of adaptation. We conclude (1) dopamine-depleted eyes are capable of photopic vision; and (2) the ERG b–wave is not diagnostic for luminosity coding at photopic backgrounds. We also predict that (1) dopamine is not required for the transition from scotopic to photopic vision in goldfish; (2) the ERG b–wave in goldfish is influenced by chromatic interactions; (3) horizontal cell spinules, though correlated with photopic mechanisms in the fish retina, are not necessary for the transition from scotopic to photopic vision; and (4) the OFF pathway, not the ON pathway, is involved in the action of dopamine on luminosity coding in the retina.

Nitric oxide (NO) is known to exert multiple effects on the function of many retinal neurons and their synapses. Therefore, it is equally important to understand the potential sources of NO within the retina. To explore this, we employ a combination of 4-amino-5-methylamino-2′,7′-difluorofluorescein diacetate (DAF-FM) based NO detection and immunohistochemistry for the NO synthetic enzymes, neuronal and endothelial nitric oxide synthase (nNOS and eNOS). We find DAF signals in photoreceptors, horizontal cells, amacrine cells, efferent synapses, Müller cells, and cells in the ganglion cell layer (GCL). nNOS immunoreactivity was consistent with the DAF signal with the exception that horizontal cells and Müller cells were not clearly labeled. eNOS-like immunoreactivity (eNOS-LI) was more widespread with photoreceptors, horizontal cells, occasional bipolar cells, amacrine cells, Müller cells, and cells in the GCL all showing labeling. Double labeling with antibodies raised against calretinin, syntaxin, and glutamine synthetase confirmed that horizontal cells, amacrine cells, and Müller cells (respectively) were expressing eNOS-LI. Although little or no nNOS labeling is observed in horizontal cells or Müller cells, the expression of eNOS-LI is consistent with the ability of these cells to produce NO. Together these results suggest that the capability to produce NO is widespread in the chicken retina. We propose that multiple forms of regulation for nNOS and eNOS play a role in the patterning of NO production in the chicken retina.

Male horseshoe crabs, Limulus polyphemus, use their eyes to locate mates day and night. We investigated their ability to detect targets of different size and contrast in a mating area of Buzzards Bay, Cape Cod, MA. We found that males can see large, high-contrast targets better than small, low-contrast ones. For targets of the same size, animals must be about 0.1 m closer to a low-contrast target to see it as well as a high-contrast one. For targets of the same contrast, animals must be approximately 0.2 m closer to a small target to see it as well as one twice as large. A decrease of 0.05 steradians in the size of the retinal image of a target can be compensated by a four-fold increase in contrast. About 60% of the animals detect black targets subtending 0.110 steradians (equivalent to an adult female viewed from about 0.56 m), while only 20% detect targets subtending 0.039 steradians. This study shows that horseshoe crabs maintain about constant contrast sensitivity under diurnal changes in light intensity in their natural environment. As a consequence of circadian and adaptive mechanisms in the retina, male horseshoe crabs can detect female-size objects about equally well day and night.

Interocular alignment was assessed by corneal light reflex photography in 15 normal and 26 strabismic kittens. Strabismus was induced at 3–4 weeks of age by severing one extraocular muscle (tenotomy), by cutting and reinserting the muscle at another position on the ocular globe (recession), or by combining recession of the medial rectus muscle with resection of the lateral rectus muscle of the same eye. Nineteen strabismic and five normal kittens were followed longitudinally from 12 days to about 6 months of age.

Three out of the six longitudinally followed tenotomized cats and six out of the 13 recessed cats conserved their postoperative ocular deviation throughout the testing period (“large-angle strabismics”). Three tenotomized and seven recessed cats showed a transient deviation for 1–2 weeks after surgery, after which the interocular deviation diminished to values found in normal cats (“microstrabismic” cats). Both recessed-resected cats showed a transient interocular deviation.

In spite of their different developmental histories, all cats showed a clear breakdown of binocularity in area 17. Large-angle strabismics showed a dominance of the non-operated eye, while in microstrabismic cats, both eyes were equally effective in driving cortical cells. It thus appears that a transient strabismus is sufficient to produce a reduction of binocularity in area 17.

Embryonic chick retinal pigment epithelial (RPE) cells can undergo transdifferentiation upon appropriate stimulation. For example, basic fibroblast growth factor (bFGF) induces intact RPE tissue younger than embryonic day 4.5 (E4.5) to transdifferentiate into a neural retina. NeuroD, a gene encoding a basic helix-loop–helix transcription factor, triggers de novo production of cells that resemble young photoreceptor cells morphologically and express general neuron markers (HNK-1/N-CAM and MAP2) and a photoreceptor-specific marker (visinin) from cell cultures of dissociated E6 RPE (Yan & Wang, 1998). The present study examined whether bFGF will lead to the same transdifferentiation phenomenon as neuroD when applied to dissociated, cultured E6 RPE cells, and whether interplay exists between the two factors under the culture conditions. Dissociated E6 RPE cells were cultured in the presence or absence of bFGF, and with or without the addition of retrovirus expressing neuroD. Gene expression was analyzed with immunocytochemistry and in situ hybridization. Unlike neuroD, bFGF did not induce the expression of visinin, or HNK-1/N-CAM and MAP2. However, bFGF elicited the expression of RA4 immunogenicity; yet, many of these RA4-positive cells lacked a neuronal morphology. Addition of bFGF to neuroD-expressing cultures did not alter the number of visinin-expressing cells; misexpression of neuroD in bFGF-treated cultures did not change the number of RA4-positive cells, suggesting the absence of interference or synergistic interaction between the two factors. Our data indicated that bFGF and neuroD induced the expression of different genes in cultured RPE cells.

In the present study, using double- or triple-label immunocytochemistry in conjunction with confocal microscopy, we aimed to examine the population and distribution of photoreceptors, GABAergic and glycinergic amacrine cells, and ganglion cells, which are basic but important parameters for studying the structure–function relationship of the salamander retina. We found that the outer nuclear layer (ONL) contained 82,019 ± 3203 photoreceptors, of which 52% were rods and 48% were cones. The density of photoreceptors peaked at ∼8000 cells/mm2 in the ventral and dropped to ∼4000 cells/mm2 in the dorsal retina. In addition, the rod/cone ratio was less than 1 in the central retina but larger than 1 in the periphery. Moreover, in the proximal region of the inner nuclear layer (INL3), the total number of cells was 50,576 ± 8400. GABAergic and glycinergic amacrine cells made up approximately 78% of all cells in this layer, including 43% GABAergic, 32% glycinergic, and 3% GABA/glycine colocalized amacrine cells. The density of these amacrine cells was ∼6500 cells/mm2 in the ventral and ∼3200 cells/mm2 in the dorsal area. The ratio of GABAergic to glycinergic amacrine cells was larger than 1. Furthermore, in the ganglion cell layer (GCL), among a total of 36,007 ± 2010 cells, ganglion cells accounted for 65.7 ± 1.5% of the total cells, whereas displaced GABAergic and glycinergic amacrine cells comprised about 4% of the cells in this layer. The ganglion cell density was ∼1800 cells/mm2 in the ventral and ∼600 cells/mm2 in the dorsal retina. Our data demonstrate that all three major cell types are not uniformly distributed across the salamander retina. Instead, they exhibit a higher density in the ventral than in the dorsal retina and their spatial arrangement is associated with the retinal topography. These findings provide a basic anatomical reference for the electrophysiological study of this species.

Recovering the velocity of objects moving in the visual field requires both the integration and segmentation of local neuronal responses elicited by moving stimuli in primary visual cortex. Herein, we investigate the effects of the contrast, density, spatial proximity, spatial frequency, and spatial configuration of component motions on these complementary processes. Measuring the ability of human observers to discriminate the global direction of motion displays composed of spatially distributed patches of drifting gratings whose motion is locally ambiguous, we provide psychophysical evidence that linking component motion across space is facilitated at low contrast and high patch density. Furthermore, direction discrimination depends on the spatial frequency of component gratings and is more accurate for spatial configurations that contain “virtual” L junctions as compared to configurations composed of “virtual” T junctions. We suggest that the conditions yielding global motion coherence can be accounted for by the existence of anisotropic cooperative/competitive, contrast-dependent, long-range interactions among oriented direction-selective units. In addition, we bring evidence that motion segmentation processes rely upon the processing of moving local spatial discontinuities. The results are discussed in the light of recent psychophysical and physiological evidence that long-range excitatory and inhibitory interactions within primary visual cortex modulate perceptual linking.

The metabotropic receptor mGluR6 is localized to the dendrites of On bipolar cells and mediates synaptic input from photoreceptors. The binding of glutamate to the receptor activates a phosphodiesterase (PDE), which then hydrolyzes cGMP. A nonselective cationic conductance, believed to be gated directly by cGMP, is turned off as a result of the fall in cGMP levels, and the cell hyperpolarizes. Here we present evidence for regulation of the conductance by an additional mechanism that it is independent of cGMP. Whole-cell recordings were obtained from On bipolar cells in slices of tiger salamander retina. Dialysis of cells with 1 μM KN-62 or 10 μM KN-93, two inhibitors of type II calmodulin-dependent protein kinase (CaMKII), depressed cGMP-dependent currents. This depression persisted when hydrolysis of cGMP was prevented with IBMX, a broad-spectrum PDE inhibitor, suggesting that CaMKII acts downstream from the PDE in the cascade. The depression of cGMP-dependent currents was probably not due to a direct interaction of the inhibitors with the channels as neither 1 μM KN-62 or 10 μM KN-93 was found to have any effect on cyclic nucleotide-gated channels when applied directly to excised patches of rod outer segments. We propose that phosphorylation by CaMKII may be an important mechanism for regulating the cGMP-dependent conductance of On bipolar cells.

Transmission through the lateral geniculate nucleus is facilitated following activation of the cholinergic input from the brain stem, which is thought to reflect activity patterns seen during arousal. One of the underlying mechanisms is the suppression of inhibitory circuits local to the lateral geniculate nucleus. However, evidence exists that some visually driven inhibitory inputs to geniculate relay cells may be preserved or even enhanced under conditions of arousal, and during electrical activation of the parabrachial region of the brain stem. We have therefore reexamined the effect of brain-stem activation on the visual responses of one group of local inhibitory inputs to geniculate relay cells, those emanating from the adjacent perigeniculate nucleus. We recorded single perigeniculate cells in anesthetized, paralyzed cats. Axons innervating the lateral geniculate and perigeniculate nuclei from the parabrachial region of the brain stem were electrically activated, and the effect of this activation was assessed on both spontaneous and visually evoked responses. Visual stimulation consisted of sinusoidally modulated sine–wave gratings of varying spatial and temporal frequency. For the great majority of perigeniculate cells (32 of 40), brain-stem activation inhibited spontaneous activity, while one cell was excited, three showed a mixed effect and four were unaffected. Nevertheless, the responses of most cells (30 of 40) were facilitated when brain-stem activation was paired with certain spatio-temporal patterns of visual stimulation. Spatial tuning curves were constructed for 17 cells and temporal tuning curves for 14, before and during parabrachial activation. The responses of any one cell could be facilitated, unchanged, or suppressed, depending on the visual stimulus used. In some cases, this substantially modified the cell’s spatial and temporal tuning properties. We conclude that activation of the brain stem disinhibits geniculate relay cells in the absence of visual stimulation, but it has the potential to enhance either the magnitude or specificity of visually driven inhibition arising from the perigeniculate nucleus.

Albino vertebrates exposed to intense light typically lose photoreceptors via apoptosis, and thus serve as useful models of retinal degeneration. In contrast, albino rainbow trout exposed to intense light maintain populations of rod and cone nuclei despite substantial damage to rod outer segments (ROS). The aim of this study was to differentiate between two hypotheses that could account for this divergent result: (1) trout rod nuclei remain intact during light damage, or (2) rod nuclei die but are replaced by cell proliferation. A further aim was to examine whether photic history modulates retinal damage, as in rodents. Albino and normally pigmented trout were moved from defined photic regimes into full daylight, while some were not moved to serve as protected controls. ROS were always maintained in pigmented fish and in albinos protected from full daylight. In albinos exposed to full daylight, ROS were removed over most of the central retina, whereas rod nuclei were maintained in the outer nuclear layer over 10 days. Pyknotic and TUNEL-labeled rod nuclei were abundant in affected albinos at all time-points tested. Rod death occurred without a decrease in the number of rod nuclei, confirming that proliferation must be replacing cells. Indeed a transient increase in proliferation was observed in retinal progenitors of albinos receiving 5 days of damaging light. This proliferative response was decreased with further damage. Cones remained intact even in areas where rod nuclei had degenerated. Pretreatment with light of moderate versus low intensity light affected the cell death and proliferative responses, and the ectopic localization of rod opsin. We conclude that apoptotic demise of rods, but not cones, occurred during light damage in retinas of albino trout and proliferative responses have a limited a capacity to replace lost rods.

Unlike the mammalian retina, the teleost fish retina undergoes persistent neurogenesis from intrinsic stem cells. In marine teleosts, most cone photoreceptor genesis occurs early in the embryonic and larval stages, and rods are added primarily during and after metamorphosis. This study demonstrates a developmental paradigm in elopomorph fishes in which retinas are rod-dominated in larvae, but undergo periods of later cone genesis. Retinal characteristics were compared at different developmental stages among three ecologically distinct elopomorph fishes—ladyfish (Elops saurus), bonefish (Albula vulpes), and speckled worm eel (Myrophis punctatus). The objectives were to improve our understanding of (1) the developmental strategy in the elopomorph retina, (2) the functional architecture of the retina as it relates to ecology, and (3) how the light environment influences photoreceptor genesis. Photoreceptor morphologies, distributions, and spectral absorption were studied at larval, juvenile, and adult stages. Premetamorphic retinas in all three species are rod-dominated, but the retinas of these species undergo dramatic change over the course of development, resulting in juvenile and adult retinal characteristics that correlate closely with ecology. Adult E. saurus has high rod densities, grouped photoreceptors, a reflective tapetum, and longer-wavelength photopigments, supporting vision in turbid, low-light conditions. Adult A. vulpes has high cone densities, low rod densities, and shorter-wavelength photopigments, supporting diurnal vision in shallow, clear water. M. punctatus loses cones during metamorphosis, develops new cones after settlement, and maintains high rod but low cone densities, supporting primarily nocturnal vision. M. punctatus secondary cone genesis occurs rapidly throughout the retina, suggesting a novel mechanism of vertebrate photoreceptor genesis. Finally, in postsettlement M. punctatus, the continuous presence or absence of visible light modulates rod distribution but does not affect secondary cone genesis, suggesting some degree of developmental plasticity influenced by the light environment.

The goal of this work was to provide a detailed quantitative description of the recepii ve-field properties of one of the types of rarely encountered retinal ganglion cells of cat; the cell named the Q-cell by Enroth-Cugell et al. (1983). Quantitative comparisons are made between the discharge statistics and between the spatial receptive properties of Q-cells and the most common of cat retinal ganglion cells, the X-cells. The center-surround receptive field of the Q-cell is modeled here quantitatively and the typical Q-cell is described. The temporal properties of the Q-cell receptive field were also investigated and the dynamics of the center mechanism of the Q-cell modeled quantitatively. In addition, the response vs. contrast relationship for a Q-cell at optimal spatial and temporal frequencies is shown, and Q-cells are also demonstrated to have nonlinear spatial summation somewhat like that exhibited by Y-cells, although much higher contrasts are required to reveal this nonlinear behavior. Finally, the relationship between Q-cells and Barlow and Levick's (1969) luminance units was investigated and it was found that most Q-cells could not be luminance units.

A circadian clock in the brain of the horseshoe crab, Limulus polyphemus, has an important role in the function of the peripheral visual system. At night, the clock transmits neural activity to the lateral, ventral, and median eyes via efferent optic nerve fibers. The activity occurs in synchronous bursts (maximum rate of 2 bursts/s) with individual efferent fibers contributing a single spike in each burst. The circadian efferent activity originates in the protocerebrum. Lateral connections synchronize the efferent activity recorded from the two halves of the protocerebrum, suggesting the existence of bilateral circadian oscillators. Circadian efferent activity survives excision of the brain and isolation of the protocerebrum. We conclude that circadian clock and its complex neural circuitry are fundamental components of the Limulus visual system.

Goodhill (1993) has recently suggested that the spacing of ocularity domains in visual cortex is not solely an intrinsic property of cortex, but is determined, at least in part, by the degree of correlation in the activity of the two eyes. In support of this model, Löwel (1994) has shown that strabismus, which decorrelates the activity of the two eyes, increases the spacing of ocular dominance columns in area 17, but not area 18, of the cat. As a further test of Goodhill's model, in this paper we examine the effects of another rearing procedure that decorrelates the activity of the two eyes, namely alternating monocular exposure (AME). Cats were reared either normally (9 cats) or with AME (21 cats). We labeled their ocularity domains by one of three methods: ocular dominance columns by 2-deoxyglucose (14 cats), and ocular dominance patches by transneuronal transport (14 cats), or by injections of tracer into single layers of the lateral geniculate nucleus (LGN; 2 cats). The spacing of ocular dominance was 11% greater in the AME cats than in the normal cats (0.976 vs. 0.877 mm). These results are similar to those previously reported for strabismic cats, although the effect is less striking. We thus confirm that decorrelating the activity of the two eyes increases the spacing of cortical ocularity domains. Our results further suggest that the degree of decorrelation affects the extent of that increase.

Dendrites of retinal ganglion cells (RGCs) tend to be distributed preferentially toward areas of reduced RGC density. This, however, does not occur in the retina of normal pigmented rats, in which it has been suggested that the centro-peripheral gradient of RGC density is too shallow to provide directional guidance to growing dendrites. In this study, laterally displaced dendrites of RGCs retrogradely labeled with horseradish peroxidase were related to cell density gradients induced experimentally in the rat retina. Neonatal unilateral lesions of the optic tract produced retrograde degeneration of contralaterally projecting RGCs, but spared ipsilaterally projecting neurons in the same retina. These lesions created an anomalous temporal to nasal gradient of cell density across the decussation line, opposite to the nasal to temporal gradient found along the same axis in either normal rats or rats that had the contralateral eye removed at birth. RGCs in rats that received optic tract lesions had their dendrites displaced laterally toward the depleted nasal retina, while in either normal or enucleated rats there was no naso-temporal asymmetry. The lateral displacement affected both primary dendrites and higher-order branches. However, the gradient of cell density after optic tract lesions was less steep than the gradient in either normal or enucleated rats. To test for the presence of steeper gradients at early stages of development, RGC density gradients were also examined at postnatal day 5 (P5). In normal rats, the RGCs were homogeneously distributed throughout the retina, while rats given optic tract lesions at birth already showed a temporo-nasal density gradient at P5. Still, this anomalous gradient was less steep than that found in normal adults. It is concluded that the time course, rather than the steepness of the RGC density gradient, is the major determinant of the lateral displacement of dendritic arbors with respect to the soma in developing RGCs. The data are consistent with the idea that the overall shape of dendritic arbors depends in part on dendritic competition during retinal development.

The morphology of retinal ganglion cells within the central retina during formation of the fovea was examined in retinal explants with horseradish-peroxidase histochemistry. A foveal depression was first apparent in retinal wholemounts at embryonic day 112 (El 12; gestational term is approximately 165 days). At earlier fetal ages, the site of the future fovea was identified by several criteria that included peak density of ganglion cells, lack of blood vessels in the inner retinal layers, arcuate fiber bundles, and the absence of rod outer segments in the photoreceptor layer. Prior to E112, the terminal dendritic arbor of retinal ganglion cells within the central retina extended into the inner plexiform layer and were located directly beneath their somas of origin or at most were slightly displaced from it. For example, at E90 the mean horizontal displacement of the geometric center of the dendritic arbor from the somas of cells within 600 μm of the estimated center of the future fovea was 4.1 μm (S.D. 2.7, range 1.0-10.0, n = 97). Following formation of the foveal depression the dendritic arbors of cells were significantly displaced from their somas. For example, at E138 the mean displacement was 41.2 μm (S.D. 12.2, range 12.0-56.0, n = 97). The displacement of the dendritic arbor which occurred during this period was not accounted for by areal growth of the dendritic arbor, the somas, or the retina, but was produced by the lengthening of the primary dendritic trunk. Moreover, no significant displacement was observed within the remaining 1.5–6.5 mm of the central retina. These observations provide evidence supporting early speculations that the formation of the foveal pit occurs, in part, by the radial migration of ganglion cells from the center of the fovea during its formation. Our analyses suggest that this migration occurs by the lengthening of the primary dendrite presumably by the addition of membrane. This migration is in a direction opposite to the inward movement of photoreceptors that occurs during late fetal and early postnatal periods (Packer et al., 1990, Journal of Comparative Neurology 298, 472–493).

Parvocellular (P-) and magnocellular (M-) cells in the marmoset LGN can receive prominent rod input up to relatively high illuminance levels (Kremers et al., 1997b). In the present paper, we quantify rod and cone input strengths under different retinal illuminance levels. The stimulus was based on the so-called “silent substitution” method. The activities of P- and M-cells of dichromatic animals were recorded extracellularly. We were able to adequately describe the response amplitudes and phases by a vector summation of rod and cone signals. At low retinal illuminance levels, the cells' responses were determined by rod and cone inputs. With increasing illuminances the strength of the cone input increased relative to the rod strength. But, we often found significant rod inputs up to illuminances equivalent to 700 td in the human eye or more. Rod input strength was more pronounced in cells with receptive fields at large retinal eccentricities. The phase differences between rod and cone inputs suggest that the rod signals lag about 45 ms behind the cone signals.

Onset and offset of calcium current in response to short, depolarizing voltage pulses were studied in giant synaptic terminals of goldfish bipolar neurons. Tail-current decays were extremely rapid (80 μs at −70 mV), and exponentially slowed at more positive repolarization potentials. The amplitude of tail current following voltage pulses varied with the pulse amplitude, according to a Bolzmann distribution with a V1/2 of −27.6 mV and a slope factor of 13.8 mV. When interpreted with a Hodgkin-Huxley model, calcium-current onset was best described by m2 kinetics and a time constant (τm) of 0.62 ms at −10 mV. The kinetics of calcium-current onset and offset are at least two- to threefold faster than those described in other native cells. Combined with other recent data, the results suggest that the rapid kinetics may participate in a fast signaling mode in the goldfish ON-center pathway.

The mesencephalic tectum plays a prominent role in integrating both visual and multimodal sensory information essential for normal behavior in amphibians. Activity in the mesencephalic tectum is thought to be modulated by the influence of distinct neurochemical inputs, including the catecholaminergic and the cholinergic systems. In the present study, we have investigated the distribution and the origin of the catecholaminergic innervation of the mesencephalic tectum in two amphibian species, the anuran Rana perezi and the urodele Pleurodeles waltl. Immunohistochemistry for dopamine and two enzymes required for the synthesis of catecholamines, tyrosine hydroxylase (TH) and dopamine β-hydroxylase (DBH), revealed a complex pattern of catecholaminergic (CA) innervation in the anuran and urodele mesencephalic tectum. Dopaminergic fibers were primarily present in deep tectal layers, whereas noradrenergic (DBH immunoreactive) fibers predominated in superficial layers. Catecholaminergic cell bodies were never observed within the tectum. To determine the origin of this innervation, applications of retrograde tracers into the optic tectum were combined with immunohistochemistry for TH. Results from these experiments demonstrate that dopaminergic neurons in the suprachiasmatic and juxtacommissural nuclei (in Rana) or in the nucleus pretectalis (in Pleurodeles), together with noradrenergic cells of the locus coeruleus, are the sources of CA input to the amphibian mesencephalic tectum. The present results suggest that similar CA modulatory inputs are present in the mesecencephalic tectum of both anurans and urodeles.

We performed a nonradioactive in situ hybridization histochemistry (ISH) study of the lateral geniculate nucleus (LGN) and the primary visual area (area 17) of the macaque monkey to investigate mRNA expression of the myristoylated alanine-rich C-kinase substrate (MARCKS), a major protein kinase C (PKC) substrate. In the LGN, intense hybridization signals were observed in both magnocellular neurons (layers 1 and 2) and parvocellular neurons (layers 3 to 6). Double labeling using ISH and immunofluorescence revealed that MARCKS mRNA was coexpressed with the α-subunit of type II calcium/calmodulin-dependent protein kinase, indicating that MARCKS mRNA is also expressed in koniocellular neurons in the LGN. GABA-immunoreactive neurons in the LGN did not contain MARCKS mRNA, indicating that MARCKS mRNA is not expressed in inhibitory interneurons. The signals were generally weak in area 17, and intense signals were restricted to large neurons in layers IVB, V, and VI. GABA-immunoreactive neurons in layers II–VI of area 17 did not contain MARCKS mRNA. Double-label ISH revealed that MARCKS mRNA was coexpressed with mRNA of GAP-43, another PKC substrate, in neurons of both the LGN and area 17. To determine whether the expression of MARCKS mRNA is regulated by retinal activity, we performed ISH in the LGN and area 17 of monkeys deprived of monocular visual input by tetrodotoxin. After monocular deprivation for 5 to 30 days, MARCKS mRNA was down-regulated in the LGN, but not in area 17. These results suggest that MARCKS mediates the activity-dependent changes in the excitatory relay neurons in the LGN.