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. 2012 Oct 16;3:1136. doi: 10.1038/ncomms2136

Figure 1. Effects of FAAH-1 and AEA on axon regeneration in C. elegans.

Figure 1

(a) Schematic diagram of the JNK MAPK pathway involved in axon regeneration in C. elegans. SVH-1 growth factor and SVH-2 receptor tyrosine kinase positively regulate the JNK pathway. VHP-1 MAPK phosphatase negatively regulates it. (b) Structure of FAAH-1. Comparison between C. elegans FAAH-1 and human FAAH1 is shown. TM represents the putative transmembrane domain. The bold line underneath indicates the extent of the deleted region in the faah-1(tm5011) mutation. (c) Representative D-type motor neurons in wild-type and faah-1 mutant animals 24 h after laser surgery. Young adult animals were treated with ethanol or AEA for 6 h after axotomy. In wild-type animals, severed axons have regenerated growth cones (arrowheads). In faah-1 mutants and AEA-treated wild-type animals, severed axons failed to regenerate (arrows). Scale bars=10 μm. (d) Percentages of axons that had initiated regeneration 24 h after laser surgery. Young adult animals were treated with ethanol, AEA or EPEA for 6 h after axotomy. At least 30 axons per treatment group were assayed. (e) Effect of age on axon regeneration. Animals in L4 or young adult (YA) stage were treated with ethanol (−AEA) or AEA for 6 h after axotomy. Error bars indicate 95% confidence intervals (CI). *P<0.05, ***P<0.001 as determined by Fisher's exact test. NS, not significant.