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. Author manuscript; available in PMC: 2010 Sep 1.
Published in final edited form as: Neurotoxicology. 2009 May 4;30(5):794–802. doi: 10.1016/j.neuro.2009.04.006

Figure 6. Defects in neural patterning and axon outgrowth in the PNS of MeHg treated embryos.

Figure 6

Figure 6

Patterning of stage 14–15 embryos PNS neurons with control (A) and MeHg (50μM) exposure (B) is revealed with the anti-elav antibody. The dorsal (d), lateral (l) and ventral (v) clusters of the PNS sensory neurons form in a stereotypical pattern in each abdominal segment (A, A′) that is disrupted with MeHg exposure (B, B′). The lateral lch5 neuron cluster is denoted by (*). (Note, the intensity difference of the VNC staining arises from the slightly different orientation of the embryos in A versus B) The frequency of the MeHg-induced PNS phenotype at various MeHg concentrations is seen in the table (C) (see methods). Average and standard deviation of three independent MeHg treatments for each concentration are shown with n=150 embryos for each data point. Axon projections of stage 14–15 embryo PNS neurons with control (D) and MeHg (50μM) treatment (E) are revealed by staining with the 22C10/Futstch antibody. Normal projections of the segmental and intersegmental nerves (white arrows, D′) in control embryos and the abnormal projection of the dorsal nerve (* E′) with MeHg are shown. (Anterior is to the left and dorsal is up. See text for discussion).