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PubMed1989

Extrinsic determinants of retinal ganglion cell development in primates.

As in all mammals studied to date, primate retina contains morphologically distinct classes of retinal ganglion cells (Polyak: The Retina. Chicago: University of Chicago Press, '41; Boycott and Dowling: Philos. Trans. R. Soc. Lond. [Biol.] 225:109-184, '69; Leventhal et al.: Science 213:1139-1142, '81; Perry et al.: Neuroscience 12:1101-1123, '84; Rodieck et al.: J. Comp. Neurol. 233:115-132, '85; Rodieck: In H.D. Steklis and J. Erwin (eds): Comparative Primate Biology, Volume 4: Neurosciences. New York: Alan R. Liss, Inc., pp. 203-278, '88). We have now studied the morphologies, central projections, and retinal distributions of the major morphological classes of ganglion cells in the normal adult monkey, the newborn monkey, and the adult monkey in which restricted regions of retina were depleted of ganglion cells at birth as a result of small lesions made around the perimeter of the optic disc. Both old-world (Macaca fascicularis) and new-world (Saimiri sciureus) monkeys were studied. Our results indicate that, at birth, the major morphological classes of monkey retinal ganglion cells are recognizable; cells in central regions are close to adult size whereas cells in peripheral regions are much smaller than in the adult. As in the adult (Stone et al.: J. Comp. Neurol. 150:333-348, '73), in newborn monkeys there is a very sharp division between ipsilaterally and contralaterally projecting retinal ganglion cells (nasotemporal division). Consistent with earlier work (Hendrickson and Kupfer: Invest. Ophthalmol. 15:746-756, '76) we find that the foveal pit in the neonate is immature and contains many more ganglion cells than in the adult. In the adult monkey in which the density of retinal ganglion cells in the central retina was reduced experimentally at birth, the fovea appeared immature, and an abnormally large number of retinal ganglion cells were distributed throughout the foveal pit. The cell bodies and dendritic fields of ganglion cells that developed within cell-poor regions of the central retina were nearly ten times larger than normal. In peripheral regions the effects were smaller. The dendrites of the abnormally toward the foveal pit. They did not extend preferentially into the cell-poor region as do the abnormally large cells on the borders of experimentally induced cell-poor regions of cat central retina (Leventhal et al.: J. Neurosci. 8:1485-1499, '88) or, as we found here, in paracentral regions of primate retina.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1990

Further study of the outward displacement of retinal ganglion cells during optic nerve regeneration, with a note on the normal cells of Dogiel in the adult frog.

In a previous study we observed massive retinal ganglion cell death in adult Rana pipiens after periods of optic nerve regeneration, and reported that large numbers of the surviving cells had become displaced bodily into the inner plexiform layer of the affected eye (Scalia et al.: Brain Research 344:267-280, 1985). The outwardly displaced cells could be identified as retinal ganglion cells because they could be back-filled with horseradish peroxidase (HRP) injected into the regenerated optic nerve. Quantitative observations on the abnormal outward displacement of ganglion cells are reported here. Parallel observations on normally displaced ganglion cells (cells of Dogiel) are also reported to clarify the distinctions between these two classes of cells. For the present work, injections of HRP of varying size were placed in the optic tectum bilaterally in 3 normal frogs and 9 frogs sustaining unilateral optic nerve regeneration. Most injections were centered at loci mapping the middle region of the nasal retina. The retinas were examined as flat-mounts and in-section. In 8 other frogs sustaining optic nerve regeneration, the HRP was administered bilaterally directly to the optic nerves in the orbit. Ganglion cells were labeled by retrograde transport of the HRP in the retinal ganglion cell layer in both the normal and affected eyes in areas topographically isomorphic with the tectal areas subtended by the injections. In the normal eyes, the orthotopic ganglion cells formed a strict monolayer, and virtually no cells existed in the inner plexiform layer. In the retinas sustaining optic nerve regeneration, the retinal ganglion cells abnormally displaced into the inner plexiform layer were also labeled topographically in correspondence with the injection sites. The abnormally displaced cells comprised 5.5% of the total population of surviving neurons in the retinal ganglion cell and inner plexiform layers. The mean outward dislocation of the displaced cells, as measured in one frog surviving optic nerve crush for 8 weeks, was 69.9 +/- 2.4% of the distance across the inner plexiform layer, which itself was uniformly 14.3 +/- 0.39 microns thick. Cells of Dogiel, which were embedded within the inner nuclear layer, were also labeled when the injections of HRP spread to include the area of representation of the optic disc. The labeled cells were restricted to a dorsal, peripapillary locus capping the optic disc. Therefore, some cells of Dogiel project to the tectum normally, but only from the central retina.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Ocular↗
PubMed1992

Topographic organization of the cochlear spiral ganglion demonstrated by restricted lesions of the anteroventral cochlear nucleus.

The morphological organization of the central projections of the cat cochlear spiral ganglion into the cochlear nucleus has been investigated by creating restricted lesions in the anteroventral cochlear nucleus (AVCN) in order to ablate selectively either the lateral or the medial aspect of isofrequency projection laminae. Such lesions induced highly selective retrograde degeneration of spiral ganglion cells. Ablation of the lateral part of the AVCN resulted in degeneration of cells within the scala tympani portion of the ganglion, whereas medial lesions within the AVCN induced degeneration of the scala vestibuli portion of the ganglion. Since most, if not all, of the primary afferent axons of the cochlear nerve bifurcate into ascending and descending branches as they enter the brainstem, it is noteworthy that selective damage to the ascending branch in the AVCN was sufficient to induce retrograde degeneration of the spiral ganglion cell somata. The peripheral and central axons also degenerated, and the losses of both the radial nerve fibers in the osseous spiral lamina and the central axons passing into the modiolus displayed selective topographies that paralleled the cell loss within the spiral ganglion. The results of this study support our previous hypothesis, based upon earlier horseradish peroxidase labeling experiments, that there is a topographic organization to the projection of the spiral ganglion within the isofrequency laminae that is orthogonal to the frequency representation within the ventral cochlear nuclei (VCN). That is, in addition to the spiral frequency organization of the ganglion, represented by the dorsal-to-ventral frequency map in the VCN, there is also an orderly and sequential distribution of inputs from the vertical (scala tympani-to-scala vestibuli) dimension of the spiral ganglion across the lateral-to-medial axis of the VCN. The interaction of these two topographic representations, distributed across the three dimensions of the VCN, must partly define the selective and/or integrative neuronal response properties at this first level of central nervous system processing of auditory signals within the cochlear nuclei.

Animals↗
PubMed1994

Birthdates of neurons in the retinal ganglion cell layer of the ferret.

The present study determined the temporal and spatial patterns of genesis for neurons of different sizes in the retinal ganglion cell layer of the ferret. Fetal ferrets were exposed to tritiated thymidine on embryonic days E-22 through E-36. One to 3 months after birth, they were perfused and their retinae dissected, and autoradiographs were prepared from resin-embedded sections throughout the entire flattened retinal ganglion cell layer. Soma size differences in conjunction with separate retrograde labeling and calbindin immunocytochemical studies were used as criteria for identifying different retinal ganglion cell subtypes in juvenile and adult ferrets. Neurons of different sizes in the ganglion cell layer were generated at different stages during development. Medium sized cells were generated primarily between E-22 and E-26; the largest cells were generated between E-24 and E-29; small cells were generated between E-26 and E-32; and very small cells were generated between E-29 and E-36. The former three groups were interpreted to be three subtypes of retinal ganglion cells, while the latter group was interpreted to be displaced amacrine cells. This temporal order of the genesis of ganglion cell classes is consistent with the spatial ordering of their fibers in the mature optic chiasm and tract, and it is consistent with the developmental change in decussation pattern recently shown in the optic pathway of embryonic ferrets. The spatial pattern of genesis suggests that ganglion cells of a particular class are added to the ganglion cell layer in a centroperipheral fashion initiated in the dorsocentral retina nasal to the area centralis. No evidence was found for a wave of ganglion cell addition that proceeded in a spiralling pattern around the area centralis, as has been reported in the cat.

Animals↗
PubMed1995

Development of neuropeptide Y immunoreactive amacrine and ganglion cells in the pre- and postnatal cat retina.

In the adult cat, neuropeptide Y (NPY) immunoreactivity (IR) is found within a subgroup of gamma-type ganglion cells and a large group of regularly arrayed amacrine cells. To examine the development of these two cell groups, we charted the appearance and maturation of neuropeptide Y immunoreactivity in the pre- and post-natal cat retina. Neuropeptide Y immunoreactivity is first observed at the central retina within the ganglion cell layer on embryonic day 46, and immunoreactivity within amacrine cells of the inner plexiform layer is present by E50. The number of immunoreactive profiles reaches the adult level in the amacrine population first (around P7), while the ganglion cell population shows a protracted development, with new cells being added until the third postnatal week. NPY-immunoreactive profiles in the ganglion cell layer were confirmed to be ganglion cells by retrograde labeling in both pre- and post-natal animals. Thus, neuropeptide Y-immunoreactive ganglion cells and amacrine cells attain their mature state with very different timecourses, although both cell groups initially follow a central to peripheral pattern of development. Interestingly, NPY expression within the ganglion cell population is temporally correlated with retinal synaptogenesis in the inner plexiform layer. As in the adult cat, NPY-immunoreactive ganglion cells never show a regular distribution during development, while NPY-IR amacrine cells are always distributed regularly even at the earliest ages. The prenatal presence of a regular distribution of NPY-IR amacrine cells suggests that these cells may participate in establishing the ganglion cell mosaics that appear during postnatal development.

Animals↗
PubMed1993

NMDA receptor blockade alters the topography of naturally occurring ganglion cell death in the rat retina.

During the first 10 days after birth around half the rat's retinal ganglion cells die. Previous work has shown that ganglion cells whose axons have made large topographic targeting errors are preferentially eliminated during this period and that the selection of such cells for preferential elimination is dependent on an activity-driven mechanism: this process is one way in which the postnatal refinement of the topography of the retinocollicular projection is achieved. We have given systemic injections of the NMDA channel blocker MK801 during the first 14 days of life to see whether this activity-dependent process works via the NMDA channel. We assessed the topographic pattern of retinal ganglion cell death by making localized injections of fast blue into the superior colliculus at birth and measuring the distribution of labeled ganglion cells either at Postnatal Day 2 or at Day 14. We find that overall retinal ganglion cell death, measured by optic nerve axon counts, is not prevented by MK801 treatment. However, whereas in untreated animals ganglion cells whose axons have reached the most topographically inappropriate target area are preferentially eliminated, in MK801-treated animals ganglion cell death appears to be random, in that we see no evidence of the preferential elimination of retinal ganglion cells whose axons have made large topographic targeting errors in MK801-treated animals. NMDA receptor blockade therefore has the same effect on the pattern of retinal ganglion cell death as tetrodotoxin blockade of the retina.

Amidines↗
PubMed1995

Influence of peripheral nerve grafts on the expression of GAP-43 in regenerating retinal ganglion cells in adult hamsters.

We have examined the ability of axotomized retinal ganglion cells in adult hamsters, to regenerate axons into a peripheral nerve graft attached to the optic nerve and the expression of GAP-43 by these neurons. We also examined the effect on these events of transplanting a segment of peripheral nerve to the vitreous body. The left optic nerves in three groups of hamsters were replaced with a long segment of peripheral nerve attached to the proximal stump of the optic nerve approximately 2 mm from the optic disc to induce regeneration of retinal ganglion cells into the peripheral nerve. An additional segment of peripheral nerve was transplanted into the vitreous of the left eye in the second group. The animals from the first and second groups were allowed to survive for 1-8 weeks and the number of regenerating retinal ganglion cells was determined by applying the retrograde tracer, Fluoro-Gold to the peripheral nerve graft and the expression of GAP-43 was studied by immunocytochemistry in the same retinas. As a control, a segment of optic nerve was transplanted into the vitreous body of the left eye in the third group of hamsters. These animals were allowed to survive for 4 weeks and the number of regenerating retinal ganglion cells was counted as in Groups 1 and 2. The percentages of the regenerating retinal ganglion cells which also expressed GAP-43 were very high at all time points in Group 1 (with no intravitreal peripheral nerve) and Group 2 (with intravitreal peripheral nerve) and at 4 weeks for the Group 3 (with intravitreal optic nerve) animals. In addition, the number of regenerating retinal ganglion cells, the number of retinal ganglion cells expressing GAP-43 and the number of regenerating retinal ganglion cells which also expressed GAP-43 were much higher in Group 2 than in Group 1 at all the time points and it was also much higher in Group 2 than in Group 3 at 4 weeks whereas there was no significant difference between the results from Groups 1 and 3 at 4 weeks. These data suggested that there was a close correlation between the number of the axotomized retinal ganglion cells regenerating axons into the peripheral nerve graft attached to the optic nerve and the expression of GAP-43.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Alterations in geniculate ganglion proteins following fungiform receptor damage.

Previous anatomical studies in rat have shown that damage produced to fungiform receptors of the anterior tongue at postnatal age 2 (P2) alters the growth and ramification of primary gustatory axons in the rostral nucleus of the solitary tract (NST). Studies employing artificial rearing (AR) procedures, which functionally deprive rat pups of orochemical stimulation during critical periods of postnatal life, produce similar alterations in the development of primary gustatory axons in the NST. Therefore, orochemical stimulation during rat's early postnatal life is necessary for normal development of primary gustatory axons in the rostral NST. One hypothesis concerning receptor-damage effects and AR effects is that receptor damage during critical periods of development may alter the regulation (i.e. transcription/translation) and/or distribution (i.e. transport) of proteins in geniculate ganglion neurons, thereby affecting growth of primary gustatory axons in the rostral NST. Specific aims of the present experiments were to comprehensively examine electrophoretic profiles of geniculate ganglion proteins following P2 receptor damage and late (> P40) receptor damage. Results show that concentrations of particular geniculate ganglion proteins are differentially altered following P2 receptor damage and late receptor damage, and that early receptor damage and late receptor damage produces distinct effects on the electrophoretic profiles of particular classes of proteins. Between the ages of P7-P38, P2 receptor damage lowers ganglion concentration of an acidic membrane glycoprotein designated as A1, with an apparent M(r) of 64-67 kDa and a pI of 4.8-5.2 P2 receptor damage also lowers ganglion concentrations of GAP-43. P2 receptor damage produces transient decreases in ganglion concentrations of NF-160, NF-200, and 8 additional acidic proteins. Three of these proteins may correspond to peripheral nerve sheath proteins analyzed in previous studies of the sciatic nerve, and one of these proteins may correspond to a 24 kDa growth-associated protein characterized in regenerating optic nerve. The time-course for changes observed in ganglion proteins following P2 damage was consistent with that observed for normal anatomical development of primary gustatory axons in both the lingual epithelium and NST. Receptor damage produced at P40 and later yielded different patterns of changes in geniculate ganglion proteins. Late receptor damage produced a transient increase in ganglion concentrations of NF-160, NF-200, GAP-43 and four additional acidic proteins within the 29-57 kDa M(r) range. Late receptor damage also produced a transient decrease in the concentrations of protein A1 and a 30 kDa protein that was not affected by P2 damage. Therefore, proteins that were preferentially affected by P2 damage may be involved in the regulation of initial axonal growth within the lingual epithelium and NST, as opposed to the structural repair or maintenance of extant axons. Relationships between normal anatomical development in peripheral and central components of primary gustatory axons are discussed in relation to availability of particular cytoskeletal and growth-associated proteins.

Animals↗
PubMed2004

Quantitative ex vivo detection of rodent retinal ganglion cells by immunolabeling Brn-3b.

To evaluate the neuroprotective potential of drug candidates to treat human glaucoma, a short-term rodent model of retinal ganglion cell death was employed. Transient ischemia applied to the rodent retina, with subsequent reperfusion for 1-4 weeks, produces an experimental retinal ganglion cell death that is quantifiable. A widely used method to detect viable retinal ganglion cells involves surgical injection of labeling compounds into the superior colliculus of the rodent brain, the retrograde transport of the compounds along the axons to the retina, and subsequent microscopic evaluation of the retina. In order to circumvent the labor intensive and invasive surgery of this method, we sought an alternative means of assessing retinal ganglion cell survival that would be more suitable for high-throughput analysis. We therefore developed a method of immunolabeling whole retinas ex vivo with an antibody to Brn-3b, an antigen expressed in a subpopulation of retinal ganglion cells, that allows for detection of a representative retinal ganglion cell population. Fluorescently tagged Brn-3b immunolabeled retinas were flat-mounted, digitally imaged, and assessed using image analysis software. We determined that 60 min of ischemia caused a 49% and a 32% decrease in Brn-3b positive retinal ganglion cells in Lewis rats after 4 weeks reperfusion, and Sprague-Dawley rats after 2 weeks reperfusion, respectively. In Swiss Webster ND4 mouse retinas subjected to 45 min ischemia and 7 days reperfusion, we found a 70% decrease in Brn-3b positive cells. Thus, ex vivo immunolabeling of retinal ganglion cells using antibody to Brn-3b provides an alternative to other methods of quantifying retinal ganglion cells.

Animals↗
PubMedDate not supplied

Effects of vasoactive intestinal peptide on ganglion cells in the rabbit retina.

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.

Adenylyl Cyclases↗
PubMedDate not supplied

Retinal ganglion cell coding in simulated active vision.

The image on the retina is almost never static. Eye, head, and body movements, and externally generated motion create rapid and continual changes in the retinal image ("active vision"). Virtually all vision in animals such as primates, which make saccades as often as 3-4 times/s, is based on information that must be derived from the first few hundred milliseconds after sudden, global changes in the retinal image. These changes may be accompanied by large changes in area mean luminance, as well as higher order image contrast statistics. This study investigated how retinal ganglion cell responses, whose response properties have been typically studied and defined in a stable stimulus regime, are affected by sudden changes in mean luminance that are characteristic of active vision. Specifically, the steady-state responses of retinal ganglion cells to static or moving square-wave grating stimuli were recorded in an isolated, superfused rabbit eyecup preparation and compared to responses after saccade-like changes in luminance. The manner of coding after luminance changes was different for different ganglion cell classes; both suppression and enhancement of responses to patterns following luminance changes were found. Brisk-transient Off cells unambiguously signaled the darkening of the overall image, but were also modulated by the subsequently appearing grating stimulus. Several types of On-center cell behavior were observed, ranging from strong suppression of the subsequent response by luminance changes, to strong enhancement. Overall, most ganglion cells distinguished static patterns after a luminance change via differences in their spike discharges nearly as well as before, although there were clear asymmetries between the On and Off pathways. Changes in mean luminance in some ganglion cells, such as On-Off directionally selective ganglion cells, could create large phase shifts in the response to patterned, moving stimuli, although these stimuli were still detected immediately after luminance changes. The results of this study show that the image dynamics of active vision may be a fundamental challenge for the visual system because of strong effects on retinal ganglion cell function. However, rapid extraction of unambiguous information after luminance changes appears to be encoded in differences in the spike discharges in different retinal ganglion cell classes. Asymmetries among ganglion cell classes in sensitivity to luminance changes may provide a basis by which some provide the "context" for interpreting the firing of others.

Animals↗
PubMed1994

PCR-based analysis of herpes simplex virus type 1 latency in the rat trigeminal ganglion established with a ribonucleotide reductase-deficient mutant.

Competitive quantitative PCR and reverse transcriptase-PCR were used to quantitate DNA and RNA from an attenuated ribonucleotide reductase-deleted herpes simplex virus type 1 (HSV-1) mutant in the rat trigeminal ganglion after peripheral inoculation following corneal scarification. Amplification of ganglionic DNA with oligonucleotide primers specific for the HSV-1 glycoprotein B (gB) gene and for the latency-associated transcript (LAT) gene indicated that there were approximately 2 x 10(5) genome equivalents per ganglion at 2 days, 7 days, and 8 weeks after inoculation. Amplification of ganglionic RNA with primers specific for HSV-1 LAT indicated that the amount of LAT RNA was also stable over 8 weeks, with 10(7) LAT molecules per ganglion at 2 days and at 7 days postinoculation and 1.4 x 10(7) LAT molecules per ganglion at 8 weeks. In situ hybridization with a digoxigenin-labeled riboprobe specific for LAT detected an average of one to two LAT-positive cells in each positive 6-microns section of trigeminal ganglion. In situ PCR detection of HSV-1 genomes in similar sections, using digoxigenin-labeled nucleotides with primers specific for HSV-1 gB, identified as many as 120 genome-positive cells per section. These results indicate that there are approximately 50 LAT molecules per latent HSV-1 genome in the trigeminal ganglion, compared with 15 LAT molecules per latent HSV-1 genome in the central nervous system (R. Ramakrishnan, D. J. Fink, G. Jiang, P. Desai, J. C. Glorioso, and M. Levine, J. Virol. 68:1864-1873, 1994), but that cells with detectable LATs by in situ hybridization represent only a small proportion of those ganglionic neurons containing HSV-1 genomes. The presence of latent HSV-1 genomes in a large number of neurons suggests that HSV-1 may be more efficient in establishing the latent state than would be anticipated from previous reports.

Animals↗
PubMed2006

Evoked expression of the glutamate transporter GLT-1c in retinal ganglion cells in human glaucoma and in a rat model.

PURPOSE: Glaucoma is a common disease of the eye, a key characteristic consequence of which is the death of retinal ganglion cells. The cause of this loss is unknown, though glutamate-mediated toxicity has been implicated. Glutamate transporters are key regulators of glutamate; therefore, the purpose of the study was to determine whether unusual excitation is associated with unusual expression of one or more transporters. METHODS: The expression of a splice variant of the glutamate transporter GLT-1 (EAAT2) was examined in normal and glaucomatous retinas from humans and rats. RESULTS: In normal eyes of humans and rats, GLT-1c was expressed only in photoreceptors. In glaucoma, there was additional robust expression of GLT-1c in retinal ganglion cells, including occasional displaced ganglion cells. Conversely, cells such as displaced amacrine cells and amacrine cells were unlabeled. CONCLUSIONS: The induction of GLT-1c expression by retinal ganglion cells supports the notion that an anomaly or anomalies in glutamate homeostasis may be evident in glaucoma and that such anomalies selectively influence retinal ganglion cells. By analogy to in vitro experiments in which elevated glutamate levels induce expression of glutamate transporters, the authors hypothesize that expression of GLT-1c may represent an attempt by retinal ganglion cells to protect themselves against elevated levels of glutamate. Such anomalies in glutamate levels cannot be restricted to the ganglion cell layer, as this would not have affected displaced ganglion cells. GLT-1c may be a useful indicator of the extent of stress of the retinal ganglion cells and thus a tool for examining outcomes of potential therapeutic and experimental interventions.

Aged↗
PubMed2001

The autoregulation of retinal ganglion cell number.

The development of the nervous system is dependent on a complex set of signals whose precise co-ordination ensures that the correct number of neurones are generated. This regulation is achieved through a variety of cues that influence both the generation and the maintenance of neurones during development. We show that in the chick embryo, stratified retinal ganglion cells (RGCs) are themselves responsible for providing the signals that control the number of RGCs that are generated, both by inhibiting the generation of new ganglion cells and by killing incoming migratory ganglion cells. Selective toxicological ablation of RGCs in the chick embryo resulted in the achronic generation of ganglion cells, which eventually led to the repopulation of the ganglion cell layer and a large decrease in the physiological cell death affecting postmitotic migratory neurones. Interestingly, the application of exogenous NGF reversed the effects of ganglion cell ablation on ganglion cell death. Because the only source of NGF in the retina is that produced by the stratified ganglion cells, we infer that these differentiated neurones regulate their own cell number by secreting NGF, a neurotrophin that has previously been shown to be responsible for the death of migrating ganglion cells.

Animals↗
PubMed2004

Evidence that each S cone in macaque fovea drives one narrow-field and several wide-field blue-yellow ganglion cells.

A rule of retinal wiring is that many receptors converge onto fewer bipolar cells and still fewer ganglion cells. However, for each S cone in macaque fovea, there are two S-cone ON bipolar cells and two blue-yellow (BY) ganglion cells. To understand this apparent rule reversal, we reconstructed synaptic patterns of divergence and convergence and determined the basic three-tiered unit of connectivity that repeats across the retina. Each foveal S cone diverges to four S-cone ON bipolar cells but contacts them unequally, providing 1-16 ribbon synapses per cell. Next, each bipolar cell diverges to two BY ganglion cells and also contacts them unequally, providing approximately 14 and approximately 28 ribbon synapses per cell. Overall, each S cone diverges to approximately six BY ganglion cells, dominating one and contributing more modestly to the others. Conversely, of each pair of BY ganglion cells, one is dominated by a single S cone and one is diffusely driven by several. This repeating circuit extracts blue/yellow information on two different spatiotemporal scales and thus parallels the circuits for achromatic, spatial vision, in which each cone dominates one narrow-field ganglion cell (midget) and contributes some input to several wider-field ganglion cells (parasol). Finally, because BY ganglion cells have coextensive +S and -(L+M) receptive fields, and each S cone contributes different weights to different BY ganglion cells, the coextensive receptive fields must be already present in the synaptic terminal of the S cone. The S-cone terminal thus constitutes the first critical locus for BY color vision.

Animals↗
PubMed1990

Topographic organization of the peripheral projections of the trigeminal ganglion in the fetal rat.

Retrograde tracing with true blue (TB) and diamidino yellow (DY) was used to determine the topography of the peripheral projections of the trigeminal (V) ganglion in rats on embryonic day 16 (E-16; E-0 was the day of conception). On E-16, the earliest age at which we were able to accomplish retrograde tracing successfully, the topographic organization of the V ganglionic projection to the periphery was quite adult-like. Cells projecting to the vibrissa pad were restricted to the ophthalmic-maxillary portion of the ganglion, with those innervating dorsal row follicles located medially and those supplying ventral row follicles located laterally. Injections of tracer into ophthalmic skin and/or the cornea labeled cells that were tightly clustered in the most dorsal and anteromedial portion of the ophthalmic-maxillary region. Injections of tracer into the lower jaw or the skin just rostral to the ear labeled cells that were restricted to the lateral, mandibular part of the ganglion. None of the combinations of injections we carried out resulted in large numbers of double-labeled V ganglion cells. Injection of TB into the vibrissa pad and DY into the upper lip produced a small number of double-labeled ganglion cells. This was also the case for paired injections of TB and DY into the lower jaw and lip, respectively. No more than 15 such cells were observed in a ganglion. These findings suggest that the substantial cell death that has been reported to occur in prenatal V ganglion development (Davies and Lumsden, 1984) is probably not involved in the correction of major peripheral targeting errors by the axons of V ganglion cells.

Animals↗
PubMed2001

A dopamine- and protein kinase A-dependent mechanism for network adaptation in retinal ganglion cells.

Vertebrates can detect light intensity changes in vastly different photic environments, in part, because postreceptoral neurons undergo "network adaptation." Previous data implicated dopaminergic, cAMP-dependent inhibition of retinal ganglion cells in this process yet left unclear how this occurs and whether this occurs in darkness versus light. To test for light- and dopamine-dependent changes in ganglion cell cAMP levels in situ, we immunostained dark- and light-adapted retinas with anti-cAMP antisera in the presence and absence of various dopamine receptor ligands. To test for direct effects of dopamine receptor ligands and membrane-permeable protein kinase ligands on ganglion cell excitability, we recorded spikes from isolated ganglion cells in perforated-patch whole-cell mode before and during application of these agents by microperfusion. Our immunostainings show that light, endogenous dopamine, and exogenous dopamine elevate ganglion cell cAMP levels in situ by activating D1-type dopamine receptors. Our spike recordings show that D1-type agonists and 8-bromo cAMP reduce spike frequency and curtail sustained spike firing and that these effects entail protein kinase A activation. These effects resemble those of background light on ganglion cell responses to light flashes. Network adaptation could thus be produced, to some extent, by dopaminergic modulation of ganglion cell spike generation, a mechanism distinct from modulation of transmitter release onto ganglion cells or of transmitter-gated currents in ganglion cells. Combining these observations with results obtained in studies of photoreceptor, bipolar, and horizontal cells indicates that all three layers of neurons in the retina are equipped with mechanisms for adaptation to ambient light intensity.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2002

How voltage-gated ion channels alter the functional properties of ganglion and amacrine cell dendrites.

The present study compares the structure and function of retinal ganglion and amacrine cell dendrites. Although a superficial similarity exists between amacrine and ganglion cell dendrites, a comparison between the branching pattern of the two cell types reveals differences which can only be appreciated at the microscopic level. Whereas decremental branching is found in ganglion cells, a form of non-decremental or "trunk branching" is observed in amacrine cell dendrites. Physiological differences are also observed in amacrine vs ganglion cells in which many amacrine cells generate dendritic impulses which can be readily distinguished from those of the soma, while separate dendritic impulses in ganglion cell dendrites have not been reported. Despite these differences, both amacrine and ganglion cell dendrites appear to contain voltage-gated ion channels, including TTX-sensitive sodium channels. One way to account for separate dendritic impulses in amacrine cells is to have a higher density of sodium channels and we generally find in modeling studies that a dendritic sodium channel density that is more than about 50% of that in the soma is required for excitatory, synaptic currents to give rise to local dendritic spike activity. Under these conditions, impulses can be generated in the dendrites and propagate for some distance along the dendritic tree. When the soma generates impulse activity in amacrine cells, it can activate, antidromically, the entire dendritic tree. Although ganglion cell dendrites do not appear to generate independent impulses, the presence of voltage-gated ion channels in these structures appears to be important for their function. Modeling studies demonstrate that when dendrites lack voltage-gated ion channels, impulse activity evoked by current applied to the cell body is generated at rates that are much higher than those observed physiologically. However, by placing ion channels in the dendrites at a reduced density compared to those of amacrine cells, the firing rate of ganglion cells becomes more physiological and the relationship between frequency and current (F/I relationship) can be precisely matched with physiological data. Recent studies have demonstrated the presence of T-type calcium channels in ganglion cells and our analysis suggests that they are found in higher density in the dendrites compared to the soma. This is the first voltage-gated ion channel which appears more localized to the dendrites than other cell copartments and this difference alone cries for an interpretation. The presence of a significant T-type calcium channel density in the dendrites can influence their integrative properties in several important ways. First, excitatory synaptic currents can be augmented by the activation of T-type calcium channels, although this is more likely to occur for transient rather than sustained synaptic currents because T-type currents show strong inactivation properties. In addition, T-type calcium channels may serve to limit the electrical load which dendrites impose on the spike initiation process and thus enhance the speed with which impulses can be triggered by the impulse generation site. This role whill enhance the safety factor for impulses traveling in the orthograde direction.

Action Potentials↗