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. Author manuscript; available in PMC: 2022 Apr 12.
Published in final edited form as: Cell Rep. 2022 Mar 29;38(13):110580. doi: 10.1016/j.celrep.2022.110580

Figure 2. Transient impairments in action potential generation in PV interneurons in all Scn1a+/− mice.

Figure 2.

(A) Representative current-clamp recordings from PV-Ins from all groups (1–5). Note that PV-Ins from all Scn1a+/− mice recorded at P16–P21, including those that did or did not survive to P35–P56, exhibited markedly abnormal excitability with action potential failure (shown in detail in 1a–c and 2a–c), while Scn1a+/− P35–P56 mice exhibit normal action potential generation and repetitive firing similar to WT P35–P56 mice.

(B) Input-output curves show steady-state firing frequency for PV-Ins from each group. Excitability of P16–P21 Scn1a+/− mice that did (SURVIVOR) and did not (SUDEP) survive to young adulthood was decreased relative to age-matched WT P16–P21 and to PV-INs from surviving Scn1a+/− P35–P56 mice. See Table S1.

(C–E) Summary data for maximal steady-state firing frequency (C), input resistance (D), and resting membrane potential (E) in PV-Ins from each group.

*p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001 via mixed-effects modeling (see STAR Methods). n.s., not significant.