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. 2020 Jun 17;40(25):4813–4823. doi: 10.1523/JNEUROSCI.0324-20.2020

Figure 5.

Figure 5.

A TTX-insensitive sodium current generates plateau potential. All recordings were performed in the presence of apamin. A, Representative TRN recordings in the presence of the L-type Ca2+ channel antagonist nimodipine (20 μm, top), in TTX (500 nm, middle), and in the presence of TTX and NMDG replacing extracellular Na+ (bottom). B, Summary data showing incidence of PF in the presence of nimodipine (Nim, n = 10), the P/Q- and N-type Ca2+ channel antagonist ω-conotoxin MVIIC (ω-Ctx, 1 μm, n = 10), TTX (n = 16), and TTX and NMDG (n = 28). Dashed line indicates incidence of PF in apamin. C, Summary data from the same cells as in B, quantifying evoked depolarization duration in each condition. Gray solid line indicates criterion for PF. *p < 0.05 compared with recordings in apamin group. #p < 0.05 compared with recordings in TTX.