The roles of myosin-II, actin filaments, and MTs in the contractile activity of GCs. (a, left) The stress field generated by a GC before and after treatment with the myosin-II inhibitor blebbistatin (Bleb, 50 µM, black line). (a, right) Total strain energy generated by GCs before and after Bleb treatment, with the red thick trace representing the average of 17 cells (individual traces in faint colors). Before averaging, data from each cell were normalized by the mean value before the drug treatment (E_pre). (b–c and e–f) Stress maps for typical neurons before and after treatment with calyculin A (CalyA; 2.5 nM), latrunculin A (LA; 1 µM), nocodazole (noc; 0.5 µM), and taxol (50 nM), respectively. (d) Line scan of the stress produced by a neuron over a 1-h duration before and after jasplakinolide treatment (jasp; 0.25 µM). (g) Changes in total strain energy (logarithmic scale, base 2) induced by seven different drugs. Each curve represents average of data from many cells (number shown) normalized before averaging. (h) Distribution of activated (phosphorylated, “p”) myosin-II (green) in three typical neurons, immunostained for phosphorylated myosin-II light chain. Note that active myosin-II is concentrated near the three CCs. White line, cell outline. (i) Quantitative assay of the p-myosin-II distribution in GCs. Immunostaining intensity of the cell along the axis of the neuron was measured and plotted. (j) Red curve represents best fit of the p-myosin-II distribution with a multi-peak Gaussian function (R = 0.78, n = 37). The data from each cell were normalized by the highest intensity observed as well as by the length of LP, soma, and TP, respectively.