Skip to main content
. 2018 Nov 5;9:4611. doi: 10.1038/s41467-018-07038-8

Fig. 3.

Fig. 3

Split-bPAC-K-mediated silencing of neurons. a Example traces illustrating light intensity-dependent inhibition of current ramp-driven AP firing in a neuron expressing split-bPAC-K. Scale bars: 5 s, 20 mV. b Changes in the rheobase following split-bPAC-K activation (n = 7–8, three cultures; 600 pA reflects no spike). c The intensity of the bPAC activation light determined the duration of spike-free intervals (n = 7–8, three cultures). d Correlation of the extent of membrane potential changes induced by split-bPAC-K activation with the resting membrane potential before the light pulse (Pearson correlation, two-tailed: p < 0.0001, R2 = 0.83). Data was pooled from experiments with 470 and 385 nm at 10 and 40 mW mm−2. e Light pulse duration-dependent peak currents at light intensities of 0.4 mW mm−2 (filled triangles) or 0.04 mW mm−2 (open triangles; n = 5–7, two cultures). f Example traces of the SthK current recorded at near-physiological temperature (35 °C) or at room temperature (20 °C) from the same cell. The sequence of recordings at high and low temperatures was randomized between cells, and parameters were normalized to room-temperature conditions for each neuron (n = 6, three cultures). One sample t-test: **p < 0.01; ***p < 0.001, ns: not significant. Scale bars in e and f: 5 s, 100 pA. Error bars in all graphs represent SEM