The developmental trajectory of ultraviolet photosensitivity in rainbow trout is altered by thyroxine.

Small (< 30 g) juvenile rainbow trout (Oncorhynchus mykiss) possess retinal photoreceptor mechanisms sensitive to ultraviolet (UV), short (S), middle (M), and long (L) wavelengths. During normal development, UV photosensitivity is lost progressively until, by approx. 60 g, individuals are no longer sensitive in the UV. This shift in spectral sensitivity is associated with the disappearance of small accessory corner cones (ACCs) from the retinal photoreceptor cell mosaic: the UV cone mechanism is lost. Exposing small (< 16 g) rainbow trout to the thyroid hormone thyroxine (T4) for a period of 6 weeks induced a precocial loss of the UV cone mechanism that was indistinguishable from the events that occur during normal development. Six weeks after termination of hormone treatment, the same individuals that had lost their UV photosensitivity after exposure to T4 once again possessed a peak in spectral sensitivity at 360 nm. ACCs had reappeared in the retinae of these fish. After 6 weeks of exposure to thyroxine, large (> 90 g) juvenile rainbow trout, which had lost their UV photoreceptor mechanism during normal development, were once again UV photosensitive and ACCs were found in their retinae. These results imply that the UV photoreceptor mechanism, although lost at one point during development, can reappear at another time during the life history of the same individual. Thyroid hormones appear to be involved in both the loss and reappearance of UV photosensitivity.