Fig. 3

a Bath application of ACh induced inward currents in all recorded NSPCs (20 out of 20). Sample traces of the muscarine- and nicotine-induced inward currents in recorded NSPCs. Significant reduction of the induced ACh currents in the presence of the α7 nicotinic receptor antagonist MLA (10 μM). Quantification of the frequency (Hz; P = 3.237E-5) and amplitude (pA; P < 0.0001) of the recorded cholinergic currents. b Exogenous application of GABA induced tonic activation of NSPCs (22 out of 22). GABAergic tonic responses were completely abolished in the presence of the GABA_A receptor antagonist, gabazine (10 μΜ). Exogenous application of muscimol (GABA_A receptor agonist) induced tonic activation of NSPCs. Quantification of the amplitude (pA; P = 7.904E-8) and duration (s; P = 1.141E-7) of the GABA-related responses. c Schematic protocol for NSPC recordings during local electrical stimulation. Ten pulses (20 Hz) were applied to increase the probability of presynaptic release. Superimposed representative sample trace (in red) out of >40 sweeps (in black) from NSPC responses under control conditions, following application of the polysynaptic blocker mephenesin, and application of the selective nicotinic receptor antagonist MLA suggesting synaptic cholinergic, but not GABAergic activation of the NSPCs. Quantification of the average number of detected EPSCs per sweep and the average amplitude of the responses in control and after the application of polysynaptic blocker (mephenesin). d Application of MLA during locomotion abolishes the regular and strong input to NSPCs, implying a predominant role of nicotinic receptors. ACh, acetylcholine; GABA, γ-aminobutyric acid; MLA, methyllycaconitine; NSPC, neural stem/progenitor cell; Nv, motor nerve recording. The dashed gray line represents the baseline. Data are presented as mean ± s.e.m. and as violin plots. ^***P < 0.001; ^****P < 0.0001; ns, not significant. For detailed statistics, see Supplementary Table 1.