Fig. 7. Short-term adaptation of responses to short (50 ms) stimuli shifted the
doseresponse curves to higher stimulus intensities. While the sensillar
potential (SP) amplitude (A) and the initial slope (B) encoded concentration
changes at doses
102 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 doseresponse 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 doseresponse 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 (AD; unadapted),
N=24 (E,F; unadapted) and N=10 (AF; adapted).
Asterisks indicate significant differences between the adapted and non-adapted
state (*P<0.05; **P
0.01; Student's
t-test).