Somatostatin-immunoreactive amacrine cells of chicken retina: retinal mosaic, ultrastructural features, and light-driven variations in peptide metabolism.

Somatostatin-like immunoreactive amacrine cells of the chicken retina have been characterized by immunohistochemistry at the light and electron microscope levels. The cell bodies were set back from the junction of the inner nuclear and inner plexiform layers, and prominent fibre plexuses were found in sublaminas 1 and 3-5 of the inner plexiform layer. The cells were distributed across the retinal surface with a centroperipheral gradient of cell density. Locally, the cells were organized in a non-random mosaic. Ultrastructurally, immunohistochemical reaction product was found throughout the cytoplasm of the cell bodies, particularly associated with membranous structures, including the cytoplasmic surfaces of the Golgi apparatus, and within large dense-core vesicles. In dendritic varicosities in the inner plexiform layer, reaction product was associated with the external surfaces of small, clear synaptic vesicles. The synaptic relationships of the somatostatin-immunoreactive terminals in sublamina 1 were distinct from those in sublaminas 3-5. Those in sublamina 1 received input predominantly, possibly exclusively, from bipolar cells. Feedback synapses onto bipolar terminals or to the other amacrine cell process at a synaptic dyad were observed. In sublaminas 3-5, input came predominantly, possibly exclusively, from other, non-immunoreactive amacrine cells, and output was primarily onto other amacrine cells. No synaptic contacts with ganglion cells or with other somatostatin-immunoreactive amacrine cells were identified. Changes in levels of somatostatin-like immunoreactivity in retinas of chicks kept on 12:12 light:dark cycles were detected by radioimmunoassay, and by light and electron microscopic immunohistochemistry. Levels of retinal somatostatin-like immunoreactivity increased in the light and decreased in the dark. The changes appear to be light-driven rather than circadian, since with prolonged exposure to light or dark, the levels of somatostatin-like immunoreactivity continued to increase or decrease until plateaus were reached. The light-driven change in levels of somatostatin-like immunoreactivity may be related to the predominance of bipolar input to the immunoreactive processes in sublamina 1 of the inner plexiform layer. The reduction in peptide levels in the dark may indicate greater release of somatostatin-like immunoreactivity from the amacrine cells in the dark, resulting in an inability of peptide synthesis to keep pace with breakdown. In the light, release of somatostatin-like immunoreactivity may be lower, leading to a net synthesis of peptide.