This was the case in every trial for all animals (Figure 2A). Which aspects of the motor and sensory
activity determine the timing of the jump? We found that the time at which the cocontraction ended (triggering) was highly correlated with take-off (ρ = 0.95, p < 10−9). Moreover, this correlation exists regardless of l/|v|, since the partial correlation coefficient between these two variables controlling for l/|v| remained high (ρpart = 0.94, p < 10−9). On average take-off occurred 36 ms after triggering (SD: 15, nL = 4, nT = 29; Figure 2B, dashed line) and 90% of the variance in the timing of take-off could be explained by the timing of triggering. At the sensory level, we found that the timing of the DCMD peak firing Topoisomerase inhibitor rate and take-off were highly correlated as well (ρ = 0.87, p < 10−9) and that the partial correlation coefficient between these variables controlling for l/|v| also remained high (ρpart = 0.73, p = 9.2 × 10−8). Epigenetics inhibitor Locusts took off on average 70 ms (SD: 13) after the DCMD firing rate peaked, regardless of l/|v| (Figure 2C, dashed line) and the timing of the peak accounted for 75% of the variance of the take-off time. Not all looming stimuli led to a final take-off. Thus,
locusts jumped with a median probability of 32%. The jump probability was significantly reduced compared to that of animals without a telemetry backpack (Fotowat and Gabbiani, 2007; median: 64%, pKWT = 0.003). Figure 3 shows a trial in which the same locust as in Figure 1 did not jump (Movie S2). It started preparing by cocontracting its hindleg
flexor and extensor muscles. However, compared to jump trials, the cocontraction started late, such that after a few spikes in the extensor, the through looming stimulus reached its full size, the DCMD firing rate declined, and the cocontraction ended. This was the case in 85% of trials without take-off, whereas in the remaining 15% the cocontraction failed to initiate altogether. Across animals, we found that cocontraction onset occurred significantly earlier relative to collision in jump trials (Figure 4A), whereas the timing of the DCMD peak itself did not change (Figure 4B). Thus, while the DCMD peak time predicts the time of take-off, it fails to predict its occurrence. Since cocontraction started earlier in jump trials, the number of extensor spikes was also significantly higher (Figure 4C). In contrast, there was no difference in the total number of DCMD spikes between jump and no-jump trials (Figure 4D), although the peak DCMD firing rate was higher in jump trials (Figure S2A). However, we found that if we started counting the DCMD spikes from cocontraction onset rather than stimulus onset (shaded areas in Figure 1 and Figure 3), their number was significantly higher in jump trials (Figure 4E). Furthermore, the number of DCMD spikes from cocontraction onset was highly correlated with the number of extensor spikes (ρ = 0.73, p < 10−9, Figure 4F), such that on average 4.