Although serotonin is thought to be a neurotransmitter in a number of retinal systems, much of the precise synaptic connectivity of serotonergic neurons is unknown. To address this issue, we used an antiserum directed against serotonin to label serotonergic bipolar and amacrine cells in the turtle retina. Light-microscopic analysis of labeled amacrine and bipolar cells indicated that both had bistratified dendritic arborizations primarily in stratum 1 and in strata 4/5 of the inner plexiform layer.

Ultrastructural analysis of the neurocircuitry of these cells indicated that the processes of labeled bipolar cells in the outer plexiform layer made basal junction contacts with photoreceptor terminals. Only in rare instances did labeled bipolar cells processes invaginate near photoreceptor ribbon synapses. Processes of labeled bipolar cells received both conventional and small ribbon synaptic contacts in the outer plexiform layer. Bipolar cell processes in stratum 1 of the inner plexiform layer synapsed onto either amacrine/amacrine or amacrine/ganglion cell dyads, and made rare ribbon synaptic contacts onto labeled amacrine cell processes. Synaptic inputs to serotonergic bipolar cells in stratum 1 were from unlabeled bipolar and amacrine cells. Bipolar cell contacts in strata 4/5 were similar to those in stratum 1, but were fewer in number and no bipolar cell inputs were seen.

Labeled amacrine cell output in both strata was onto other unlabeled amacrine cells and ganglion cells; but synaptic outputs to unlabeled bipolar cells were only seen in strata 4/5. In both strata 1 and 4/5, synaptic inputs to labeled amacrine cells were from both unlabeled amacrine cells and labeled bipolar cells. The serotonergic amacrine cells had many more synaptic interactions in stratum 1 than in strata 4/5 which supports the role of serotonergic bipolar cells in the OFF pathway of retinal processing. Interactions between serotonergic bipolar and amacrine cells may play an important role in visual processing.

The visual response to a flash given in the dark is known to saturate according to the Michaelis-Menten relationship. Nevertheless, the incremental response from increasing levels of mean luminance tends to follow a Weber-Fechner relationship well into the saturation range determined from the Michaelis-Menten results. This sensitivity transformation from Michaelis-Menten to Weber-Fechner is an important characteristic of light adaptation in the vertebrate retina. Recent studies concerning the role of calcium in photoreceptor adaptation have shown that the relaxation from peak to plateau in the response of isolated photoreceptors was absent under conditions in which adaptation was blocked. Comparing the pronounced relaxation from peak to plateau in turtle horizontal cells with the absence of such relaxation in the catfish response, we noted also that turtle incremental sensitivity shows a Weber-Fechner relationship while catfish incremental sensitivity more closely follows the local slope of the Michaelis-Menten relation. Based on these observations, we have obtained an expression to relate the relaxation from peak to plateau with the sensitivity transformation. We assume that adaptation shifts the half-maximum point of the Michaelis-Menten curve so that the light response relaxes to a plateau value equal to a specified fraction φ of the peak response. We show that this manipulation alone results in a transformation from Michaelis-Menten kinetics to Weber-Fechner sensitivity.