Fig. 6: Contribution of dendritic ion channels to plateau potentials.

a Plateau potentials were evoked by concurrent optogenetic stimulation to the soma (30 ms) and EFS-triggered synaptic inputs (0.1 ms). Channel blockers: D-AP5 (50 µM, n = 6 cells from 5 animals), TTX (20 nM, n = 4 cells from 3 animals), and Ni²⁺ (100 µM, n = 4 cells from 4 animals) were compared to the vehicle control (n = 11 cells from 8 animals). Sample traces overlaid with the paired baseline trace measured from the same cell (gray). Fluorescence measured in a distal dendrite ( > 200 µm from the soma). bQuantification of effects in (a). Box plots show median, 25th and 75th percentiles, and extrema. ***p < 0.001 vs. control, one-way ANOVA with Bonferroni’s post hoc test (p = 3.6 ×10⁻⁷, 8.8 ×10⁻⁸, and 1.8 ×10⁻⁸ for D-AP5, TTX, and Ni²⁺ vs. Control). c Example traces of a complex spike at the soma (orange) and simultaneously recorded plateau potential in the distal dendrites (purple). Overlaid shading qualitatively indicates dominant contributions of distinct dendritic ion channels. bAP propagation within dendrites is initially limited by A-type K_V channel activation. The initial bAPs combine with synaptic depolarization to inactivate A-type K_V channels, allowing subsequent bAPs to evoke Na_V-based dSpikes. These dSpikes lead to VGCC-dependent calcium spikes, causing prolonged dendritic membrane depolarization ( > 20 ms). In the presence of glutamate from presynaptic inputs, this prolonged depolarization efficiently engages NMDARs, resulting in a global plateau potential. Source data for Fig. 6b are provided as a Source Data file.