Fig. 5: JNK activity modulates neuronal firing.

a Representative traces of endogenously produced cholinergic SRCs from aCC/RP2 motoneurons in late stage 17 embryos in control (RN2-Gal4 / CyO) and experimental lines (RN2-Gal4 > UAS-HepCA). Scale Bar: 20 pA / 2 s. b No significant difference in SRC amplitude (21.7 ± 3.0 vs. 17.0 ± 3.1 pA / pF, control (n = 9) (gray) vs. RN2-Gal4 > UAS-HepCA (n = 9) (green) respectively, p = 0.28) or frequency (16.3 ± 3.3 vs. 15.4 ± 2.4 per min, p = 0.83) was observed. c Representative traces of endogenously produced cholinergic EPSPs from aCC/RP2 motoneurons in late-stage 17 embryos in control (RN2-Gal4 / CyO) and experimental lines (RN2-Gal4 > UAS-HepCA). Action potentials are indicated by dots. The amplitude of the action potentials is shunted because of the underlying depolarization. Scale Bar: 10 mV / 100 ms. d Motoneuron resting membrane potential (RMP) is significantly hyperpolarized in RN2-Gal4 > UAS-HepCA (−57.0 ± 7.6 vs. −81.5 ± 2.9 mV, control (n = 6) (gray) vs. RN2-Gal4 > UAS-HepCA (n = 7) (green) respectively, **p = 0.009). Consequently, the average number of action potentials fired per EPSP was also significantly reduced (20.6 ± 2.4 vs. 9.3 ± 1.7 spikes per EPSP, **p = 0.003). All data points are shown on graphs, bars represent mean ± sem.