Synaptic Inputs to ON Parasol Ganglion Cells in the Primate Retina

Abstract

In primates, the retinal ganglion cells that project to the magnocellular layers of the lateral geniculate nucleus have distinctive responses to light, and one of these has been identified morphologically as the parasol ganglion cell. To investigate their synaptic connections, we injected parasol cells with Neurobiotin in lightly fixed baboon retinas. The five ON-center cells we analyzed by electron microscopy received approximately 20% of their input from bipolar cells. The major synaptic input to parasol cells was from amacrine cells via conventional synapses and, in this respect, they resembled alpha ganglion cells of the cat retina. We also found the gap junctions between amacrine cells and parasol ganglion cells that had been predicted from tracer-coupling experiments. To identify the presynaptic amacrine cells, ON-center parasol cells were injected with Neurobiotin and Lucifer yellow in living macaque retinas, which were then fixed and labeled by immunofluorescence. Two kinds of amacrine cells were filled with Neurobiotin via gap junctions: a large, polyaxonal cell containing cholecystokinin and a smaller one without cholecystokinin. There were also appositions between cholecystokinin-containing amacrine cell processes and parasol cell dendrites. Cholinergic amacrine cell processes often followed parasol cell dendrites and made extensive contacts. In other mammals, the light responses of polyaxonal amacrine cells like these and cholinergic amacrine cells have been recorded, and the effects of acetylcholine and cholecystokinin on ganglion cells are known. Using this information, we developed a model of parasol cells that accounts for some properties of their light responses.

Cellular Basis for Contrast Gain Control over the Receptive Field Center of Mammalian Retinal Ganglion Cells

“…This might seem surprising in light of the correlation between mammalian ganglion cell types that show strong gain control and those that receive a large degree of amacrine cell input (Shapley and Victor, 1978;Freed and Sterling, 1988;Benardete et al, 1992;Kolb and Nelson, 1993;Weber and Stanford, 1994;Jacoby et al, 1996Jacoby et al, , 2000. Our results are consistent, however, with studies in salamander, which showed that gain control in ganglion cells can be explained primarily by gain control in presynaptic bipolar cells (Kim and Rieke, 2001;Rieke, 2001).…”

Identification of myopia-associated WNT7B polymorphisms provides insights into the mechanism underlying the development of myopia

“…Together with our findings indicating that WNT7B was localized to retinal ganglion cells and that its expression was significantly upregulated in experimental myopic eyes, these data support the hypothesis that WNT7B and GJD2 co-operatively regulate the normal growth of the eye through interactions between the alpha-ganglion cells and AII amacrine cells. Interestingly, alpha-ganglion cells are predominantly observed in the peripheral retina and have large dendritic regions to receive inputs from amacrine cells 47,[53][54][55][56][57] . The hypothesis that alpha- ganglion cells and AII amacrine cells are implicated in emmetropization is consistent with the peripheral defocus theory, a theory of myopia development that has been supported by clinical evidence [58][59][60][61] .…”

Molecular Phenotyping of Retinal Ganglion Cells

“…At this eccentricity (ϳ2 mm below the streak), all cells with mean diameters Ͻ8 m are amacrine cells on the basis of signatures. Brace, 1992;Penn et al, 1994;Jacoby et al, 1996;Stafford and Dacey, 1997;Xin and Bloomfield, 1997). Most amacrine cells are GABA immunoreactive, and GABA-immunoreactive dendrites comprise ϳ80% of the mass of the inner plexiform layer (Marc, 1992(Marc, , 1999bMarc et al, 1995Marc et al, , 1998.…”