Fig. 3
CGINs co-release ACh and GABA in control and 6-OHDA-treated mice. a Monosynaptic, b polysynaptic, or c mixed GABAergic PSCs evoked in postsynaptic whole cell recorded CGIN2 in response to optogenetic stimulation of presynaptic CGIN1 (control mice). c Left: Nicotinic receptor antagonists (MEC (10 µM), MLA (0.1 µM), and DHβE (10 µM)) blocked the polysynaptic but not the monosynaptic GABAergic PSC. Adding gabazine (5 µM) blocked the monosynaptic component. Right: Superimposed and normalized polysynaptic and monosynaptic GABAergic PSCs at extended scale. d Representative image of two identified biocytin-filled, monosynaptically-connected CGINs. e Left: Outward (GABAergic) and inward (cholinergic) PSCs evoked in postsynaptic CGIN2 (bottom) in response to a presynaptic spike generated in CGIN1 (top); right: same traces at an extended time scale. f Individual and averaged synaptic delays and amplitudes of GABAergic and cholinergic PSCs. g Blockade of inward and outward PSCs by nicotinic receptor antagonists and gabazine, respectively. h Representative reconstructed CGINs dendritic trees from control and 6-OHDA-treated mice. i Sholl analysis of CGINs dendrites from control and 6-OHDA-treated mice. Scale bar: d 50 µm and h 50 µm. All means ± SEM. f Significance was determined by two-tailed, unpaired Student’s t-test; i data sets were analyzed using Kolmogorov-Smirnov test. See Supplementary Table 1 for statistics; NS, not significant
