Neural circuitry and light responses of the dopamine amacrine cell of the turtle retina.

PURPOSE: To understand the circuitry and electrophysiology of the dopamine cells in the turtle retina.
METHODS: Preembedding immunocytochemistry for tyrosine hydroxylase (Toh) was done on vibratome sections of turtle retina. Resultant Toh-immunoreactive (Toh-IR) amacrine cells were then serially thin-sectioned for analysis by electron microscopy (EM). Some sections of Toh-IR cells also were post-embedding immunostained for glycine and GABA content. Intracellular recordings and dye markings were made from the turtle eyecup and slice preparation to determine the light responses of cells called A28, which have the same morphology as Toh-IR amacrine cells.
RESULTS: Physiologically A28 cells were L-type (luminosity) and gave sustained depolarizing (ON-center) responses to light pulses. High intensity light pulses produced immediate transients and long depolarizations, lasting beyond the stimulus duration. An after-hyperpolarization and an antagonistic surround could be elicited. EM reconstruction of a Toh-IR cell revealed new circuitry over that described before (Pollard, J. & Eldred, W.D. (1990). J. Neurocytol. 19, 53-66). Bipolar ribbon synapses occurred in all three dendritic tiers. However, amacrine cell inputs dominated numerically (95% amacrine input, 5% bipolar input) many of them in a serial synaptic configuration. GABA+ inputs were seen but not glycine+ inputs. Output from Toh-IR profiles was primarily to large ganglion cell dendrites but also to bipolar cell axons, GABA-IR amacrines, unspecified amacrine cells and other Toh-IR dendrites.
CONCLUSIONS: The synaptology of the dopamine cells of the turtle retina suggests that sustained inhibitory amacrine cell pathways, including GABAergic pathways, are chiefly responsible for their response characteristics at low light levels. Conversely, at higher light intensities, transient excitatory amacrine cells probably have influence.