Figure EV5. Genetic inhibition of Smo suppresses epileptogenesis in mouse kindling model.

• A
  Schematic of the kindling protocol.
• B, C
  PCR analysis of lysates form the cortex or the tail tissue of wild‐type mice (WT) and mice with conditional knockout of Smo in CaMKIIα‐positive neurons (B) or Aldh1l1‐positive cells (C). The presence of the Smo ^+/fl or Smo ^fl/fl was revealed by the fragments amplified by Smo Conditional Primer (Smo Condi Primer) and Smo WT Primer (Smo ^fl/fl without a fragment). The presence of the Cre was revealed by the fragments amplified by Cre Primer (CaMK Cre Primer in B or Aldh1l1 Cre Primer in C). The ablation of Smo was revealed by the fragment amplified by recombinant primer (Rec Primer). Oil: injection of vehicle oil; Tam: injection of tamoxifen. Primers for genotyping were as published 50, 51.
• D–F
  The intensification of behavioral seizure class (D), evoked electrographic seizure duration (ESD) (E), and the number of stimulations required to reach equivalent seizure intensity (F) in the indicated control mice.
• G
  Mean electrographic seizure threshold in Oil, Tam, CaMK Oil, and CaMK Tam group littermates. Each data point represents a result from a single mouse.
• H
  Mean electrographic seizure threshold in Ctrl or Aldh1l1 group littermates. Each data point represents a result from a single mouse. Ctrl: Smo ^+/fl (n = 20); Aldh1l1: Smo ^+/fl Aldh1l1‐Cre (n = 19).

Data information: For (D–G), Oil: Smo ^fl/fl induced by vehicle oil (n = 11); Tam: Smo ^fl/fl induced by tamoxifen (n = 15); CaMK Oil: Smo ^fl/fl CaMKIIα‐Cre ^ERT2 induced by vehicle oil (n = 12); CaMK Tam: Smo ^fl/fl CaMKIIα‐Cre ^ERT2 induced by tamoxifen (n = 20). Oil, Tam, and CaMK oil groups were used as controls. Data are mean ± SEM with Student's t‐test.