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Analysis of the ASJ Neuron in C. Elegans by Femtosecond Laser Ablation

出版	Harvard University, 2009
URL	http://books.google.com.hk/books?id=8YoWzQEACAAJ&hl=&source=gbs_api

註釋In this thesis we first present the theoretical and practical background of the femtosecond laser ablation technique. We describe the origin of the intensity threshold and its contribution to localization of damage as well as the impact of the repetition rate on resolution. We present the experimental setup and some practical considerations, including the pulse energy dependence of damage, various surgery types and their associated survival rates, and different capabilities of neuronal regeneration. The remainder of the thesis describes our experiments, findings, and interpretations. We used femtosecond laser ablation within the ASJ neuron to ablate the cell bodies, sever dendrites, and sever axons to determine their contributions to the locomotion, dauer entry, and dauer exit behaviors. We find that ablation of the ASJ cell bodies in L1 and L4 rescues the unc-1(e580) locomotory defect. Because mutation of ssu-1(fc73) rescues unc-1(e580) locomotory and volatile anesthesic phenotypes, and because ssu-1 is only expressed in the ASJ neurons, it is likely that the ablative rescue of the unc-1 phenotypes is due to elimination of SSU-1. Cutting the ASJ dendrites or axons in L4 has seemingly the opposite effect as ablating the cell body, decreasing the locomotory velocity of unc-1(e580) worms. This suggests two conclusions. First, since the locomotory velocity does not increase after axon surgery (i.e., no locomotion rescue), and since unc-1 is broadly expressed, this suggests that the ASJ cell bodies secrete an SSU-1-modified signal to affect other cells involved in the unc-1 locomotion pathway. Second, the decrease in velocity might suggest that the ASJ neuron takes input through its neuronal fibers which is inhibitory for the SSU-1-modified signal.