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Fig. 6. Involvement of TRPM channels in the Zn2+-mediated augmentation of excitability in SNc dopaminergic neurons. (A) No alteration of spike frequency by the blockade of TRP channels (100 μM FFA, 0.87±0.09, n=6; 10 μM SKF96365, 1.02±0.15, n=5; 50 μM 9-phenathrol, 0.89±0.13, n=4). (B) Significant reduction of Zn2+-induced augmentation of excitability by TRP channel blockers (100 μM Zn: Control, 1.81±0.15, n=13; FFA, 1.01±0.23, n=6; SKF96365, 0.85±0.1, n=7; 9-phenathrol, 1.0±0.12, n=4; p<0.001, one-way ANOVA; *p<0.05, **p<0.01, ***p<0.001, Dunnett’s post-hoc multiple comparison test for control; Wash: Control, 1.43±0.2, n=12; FFA, 0.88±0.29, n=6; SKF96365, 1.26±0.07, n=4; 9-phenathrol, 1.23±0.12, n=4; p>0.05, one-way ANOVA). (C) Significant inhibition of VGCC currents by SKF96365. Left, in the voltage-clamp mode, the VGCC current in isolated SNc dopaminergic neurons were elicited by 200-ms step pulses to +30 mV from a holding membrane potential of −100 mV. Right, summary of the VGCC current inhibition (10 μM SKF96365, 87.38±12.12 %, n=5; 10 μM Dantrolene, 8.96±6.11 %, n=3; 50 μM FFA, 0.07±2.04 %, n=4).
Experimental Neurobiology 2019;28:578~592 https://doi.org/10.5607/en.2019.28.5.578
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