Light and dopamine modulation of on-bipolar cell telodendria number in goldfish retina

Purpose. Previous studies have shown that membrane surface of MBb1 (ON) bipolar cell (BC) axon terminals (ATs) undergo significant changes in light and dark. In the present study we examined possible light-dependent changes in BC AT telodendria, which are the sites of lateral synaptic contact. Methods. ON-BC ATs were visualized in light- or dark-adapted retinal flatmounts by incubating in mouseαProtein Kinase C (Amersham, 1:20). Telodendria extending from ATs were counted in confocal sections taken at the level of IPL sublamina b. To determine the effect of dopamine (DA) or DA antagonists on telodendria number, drugs were administered by intravitreal injection (10μl) into light- or dark-adapted fish. In some retinas, the endogenous source of DA, interplexiform cells, was removed by lesioning with 6-OHDA. The effectiveness of the lesion was determined by tyrosine hydroxylase immunohistochemistry (ETI; rabbitαTH; 1:100). Results. BC AT telodendria numbers from light-adapted retinas were significantly higher (47±0.4) than from dark-adapted retinas (2.8±0.4). Telodendria number was similar between retinas dark-adapted for up to 7 hrs, suggesting that the observed change occurred within 1 hr, and was complete. When dark-adapted retinas were treated with DA (10μM; 45 min) there was no difference between dark-DA-treated retinas and light-adapted retinas. The effect of DA was blocked by prior treatment with the DA D1/D2 receptor antagonist, haloperidol (HAL)(50μM). When light-adapted retinas were treated with HAL (45 min) there was no difference between light-HAL-treated retinas and dark-adapted retinas. When 6 hr dark-adapted retinas were exposed to light for 20 min, telodendria number was similar to 6 hr light-adapted retinas. This effect of light was blocked by prior treatment with HAL. Removing the endogenous source of DA by 6-OHDA lesioning eliminated light/dark differences in telodendria number. Telodendria number in both light- and dark-adapted lesioned retinas were the same as in light-adapted control retinas. Conclusions. ON-BC AT telodendria are extended in the light and retracted in the dark. Treatment with DA or DA antagonists and 6-OHDA lesioning studies indicate that these light adaptive changes are mediated by dopamine. These results suggest that lateral synaptic contacts with BCs undergo significant modification within minutes of a change in the light condition.