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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: J Neurochem. 2009 Jul 2;110(5):1648–1660. doi: 10.1111/j.1471-4159.2009.06262.x

Figure 2.

Figure 2

Abnormal axonal development in insulin-lacking photoreceptors. Rat retina amacrine (open arrows) and photoreceptor (open arrowheads) neurons were cultured with (A, B, C) or without (D, E, F) insulin, or without insulin and with 6.7 μM docosahexaenoic acid (DHA) (G, H, I) for 6 days. Phase (C, F, I) and fluorescence photomicrographs showing DAPI (B, E, H) and actin labeling with rhodamine phalloidin (A, D, G). In the presence of insulin (A–C) photoreceptor axons showed narrow “axon cones” (white arrows), while in the absence of insulin (D–F) many photoreceptors developed wide axon cones (white arrows) and showed clumps of actin in their cell body (open arrowhead) and neurite (small arrowheads). DHA addition to insulin-lacking cultures (G–I) prevented the abnormal development of photoreceptor axon cones. Note that in insulin-supplemented cultures, amacrine neurons (open arrows in A-C) developed an extensive neurite outgrowth.