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.