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. 2012 Jan;26(1):81–92. doi: 10.1096/fj.11-192914

Figure 6.

Figure 6.

Exogenous RA initiates neuritogenesis in normal adult bipolar cells and exacerbates it in LIRD retinas. A) Subretinal injection with vehicle had no obvious effect on neuritogenesis after 21 d. B) LIRD induced neuritogenesis at pLX21, as evidenced by PKCα staining. C) RA initiated rod bipolar cell neuritogenesis in control mouse retinas. D) RA accelerated neuritogenesis in LIRD mouse retinas. E) RA had no effect on neuritogenesis when it was injected at pLX7. F) Partial inhibition of neuritogenesis by citral in LIRD mouse retinas. G) Citral had no effect on neuritogenesis when it was injected at pLX7. B–G) Terminals of photoreceptors (PSD-95 staining) were retracted to the ONL paralleling with neuritogenesis by rod bipolar cells. H) Summary data (means±se) for the length of rod bipolar cell dendrites, n = 5. *P < 0.05, **P < 0.01, ***P < 0.001 vs. control (vehicle); #P < 0.05 vs. pLX21 (vehicle). I–K) Rates of neuritogenesis were slower in LIRD Rdh12−/− mice compared with LIRD Rdh12+/− mice. PKCα and PSD-95 staining was normal in control Rdh12+/− retinas (I) but demonstrated LIRD-induced neuritogenesis in the survivor zones of both Rdh12+/− (J) and Rdh12−/− retinas (K). L) Compared to LIRD Rdh12+/− mice, neuritogenesis in LIRD Rdh12−/− mice was less obvious. *P < 0.05 vs. control Rdh12+/−; #P < 0.05 vs. Rdh12+/− + pLX21. Scale bars = 20 μm.