(A) Occurrence rates of dendritic Ca2+ transients in whole-mount preparations of the wild type, dTrpA1, and painless mutants, which were evoked by IR-laser irradiations (38 mW, 1 s) onto somata. We performed one trial per cell, and the number of cells of each genotype examined are indicated above each bar. (B) Peak amplitudes in somata of individual trials are plotted. Note that Ca2+ rises in somata were slow in contrast to the sharp dendritic Ca2+ transients when somata were irradiated (cf. Figure 2A; 'soma'). The magenta dots in B indicate occurrences of dendritic Ca2+ transients; the gray dots represent those with no apparent Ca2+ transient. The peak amplitudes of these slow Ca2+ rises were significantly decreased in dTrpA1 null mutants. This result was suggestive of a contribution of a dTrpA1-mediated physiological process, although an exact mechanism underlying such slow fluctuations remains unclear. (C–E) Occurrences of dendritic Ca2+ transients in the presence of TTX or Thapsigargin treatment, which depletes the cytoplasmic Ca2+ store. We focused the IR-laser (38 mW, 1 s) onto the somata of Class IV neurons in the fillet-mounted larvae, which were pretreated with TTX and Thapsigargin (C and D, respectively). Blue traces indicate the amplitudes of Ca2+ transients of controls, whereas magenta traces indicate those with the drugs. The semitransparent traces represent amplitudes of Ca2+ transients of individual cells, and the solid traces show the average values of each group. Error bars indicate the standard deviations of the peak amplitudes of Ca2+ transients. The TTX-treatment had no effect on the occurrence and amplitude of Ca2+ transients (C), whereas the Thapsigargin-treatment only decreased the amplitude of Ca2+ transients (D). The effects of TTX was confirmed by loss of spikes. The application of TTX is indicated by a green bar above the trace (E). Fisher’s exact test (A), ANOVA and Dunnet post-hoc analysis (B), and Student’s unpaired t-test (C and D) were performed and statistical significances were assigned, *p < 0.05, **p < 0.01, ***p < 0.001. Genotype: 3×[ppk-TNXXL] (attP40)/+. To further address the contribution of Ca2+-induced Ca2+-release (CICR) from the cytoplasmic Ca2+ store to the formation of Ca2+ transients, we examined mutants for the inositol triphosphate receptor gene (Itp-r83A05616/90B.0) (Venkatesh and Hasan, 1997) or the Ryanodine receptor gene (RyRK04913/16) (Casas-Tinto et al., 2011; Gao et al., 2013). Both mutants showed Ca2+ transients with occurrence and amplitude that were not significantly different from those in the wild type (data not shown), showing that the role of CICR was negligible.