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As detailed in the Extended Results, our experiments confirm this existing model and establish the efficacy of the technique for determining the behavioral correlates of neuronal subcellular components. The locomotion of L+R whole-cell-ablated unc-1(e580) animals significantly improved compared to mock animals ( Figure?2A). Postsurgery animals exhibit both cleanly sinusoidal and kinked locomotion, indicating an incomplete restoration of coordinated locomotion. To quantify locomotion rescue, we measured the crawling speed of N2 wild-type, genetically rescued ssu-1; unc-1, mock-ablated unc-1, and whole-cell-ablated unc-1 animals following surgery [http://www.selleckchem.com/products/Erlotinib-Hydrochloride.html Erlotinib in vivo] in L1 ( Figure?2B). Among strains tested, N2 animals crawl the fastest, and unc-1 mock-ablated animals crawl the slowest, with hardly any forward movement. Genetically rescued and whole-cell-ablated unc-1 animals crawl significantly (p?[http://en.wikipedia.org/wiki/Vasopressin_receptor Vasopressin Receptor] of N2 crawling speed. We next investigated the effect of single- and double-sided whole-cell ablation. Unlike L+R whole-cell ablations, neither L nor R whole-cell ablation produces a significant difference in crawling speed from mock surgery ( Figure?2C). We also investigated whether mutation of ssu-1 and ASJ ablation rescue locomotion by coincident mechanism. The crawling speed of L+R, L, and R whole-cell-ablated ssu-1; unc-1 animals is not statistically different from [http://www.selleckchem.com/products/gsk126.html selleck compound] mock-ablated ssu-1; unc-1 animals nor from L+R whole-cell-ablated unc-1 animals ( Figure?2C). Together with ASJ-specific expression of ssu-1 ( Carroll et?al., 2006), this suggests that the rescue by whole-cell ablation is likely effected by nonspecific elimination of SSU-1. Thus, our results from whole-cell ablations indicate that the ASJ neurons are necessary for and redundantly mediate the unc-1 phenotype via an SSU-1 pathway. Next, we examined the contributions of the dendrites and axons to the unc-1 signaling pathway. To reduce axonal regeneration that occurs vigorously in the larval stages ( Gabel et?al., 2008), we performed surgery in the late L4 stage, which is also the latest time that UNC-1 is required for coordinated locomotion ( Hecht et?al., 1996). Subsequent locomotion assays yield two findings. First, animals that underwent whole-cell ablations in L4 crawl significantly (p?