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Fig. 8. Intracellular motoneuron recording does not reveal residual
stimulus-related responses after pymetrozine application. (A) Recording taken
during pymetrozine application (10–7 mol
l–1, application started 
30 s before sample shown in
Ai). Bottom trace, ramp-and-hold stimulation of femoral chordotonal organ
(fCO) (240 µm, arrow indicates fCO elongation); middle trace, intracellular
recording from FETi soma; top trace, EMG from flexor tibiae muscle. (Aii)
Brushing the abdomen (heavy arrow) leads to active movements; concomitant
synaptic input to FETi proves that the intracellular recording had not been
lost during the previous pymetrozine application. Note that the pronounced
depolarisation of FETi was transient, probably caused by the initial tonic fCO
discharge sometimes observed after pymetrozine application, and disappeared
after a few minutes. FETi membrane potential was approximately –50 mV at
rest and increased by 5.5 mV in the course of the sample recording. This
depolarisation apparently reduced and eventually prevented spike discharges
towards the end of the sample shown. (B) Stimulus-related averaging of the
intracellular FETi record before (top trace) and after (middle trace)
pymetrozine application demonstrates the absence of residual stimulus-related
input after pymetrozine. (C) Histogram of flexor tibiae activity before (top
trace) and after (middle trace) pymetrozine application illustrates the
absence of stimulus-related discharge in FETi's antagonist. B and C show data
from the same recording as in A; bottom traces as in A; note response of FETI
to fCO elongation and of flexor tibiae muscle to fCO relaxation. Scale bars:
(A) 10 mV, 5 s; (B) 5 mV, 250 ms; (C) 36 spikes bin–1 (bin
width 10 ms), 250 ms.
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