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Fig. 7. Short-term adaptation of responses to short (50 ms) stimuli shifted the dose–response curves to higher stimulus intensities. While the sensillar potential (SP) amplitude (A) and the initial slope (B) encoded concentration changes at doses >=10–2 µg bombykal, the half-time of the rising phase (t1/2 rise; C) showed no significant dose dependence. The decline of the SP back to baseline (t1/2 decline; D) was relatively slow, even at low doses. After adapting stimuli (dotted lines), the amplitude of the sensillar potential and its initial slope were reduced, while t1/2 rise was not affected. Adaptation accelerated the decline of the SP and reduced the action potential frequency computed from the first five interspike intervals (AP frequency), while the action potential latency (AP latency) increased. After adapting stimuli, the dose–response curves of those parameters that describe the initial phase of the SP were shifted to the right by approximately one log10-unit. Thus, 10 times more pheromone was needed to elicit the same response (A,B). The decline, in addition to a right-shift by more than one log10-unit, was accelerated even in the baseline region of the dose–response curve (D). The AP frequency and the AP latency were shifted by more than one log10-unit (E,F). The data were normalized to the highest response during each recording, which is the largest numerical value for those variables positively correlated to the stimulus intensity. The action potential latency and t1/2 rise, which are negatively correlated to the intensity, were inversely normalized to the smallest numerical value to focus on responses in the physiological dose range. C, control. Data represent means ± S.E.M. The stimulus duration was 50 ms. N=31 (A–D; unadapted), N=24 (E,F; unadapted) and N=10 (A–F; adapted). Asterisks indicate significant differences between the adapted and non-adapted state (*P<0.05; **P<=0.01; Student's t-test).