Fig. 3: Optogenetic inhibition of pyramidal neurons attenuates neocortical seizures with narrow therapeutic window.
From: Activated astrocytes attenuate neocortical seizures in rodent models through driving Na+-K+-ATPase
a Left panel, schematic of viral injection, stimulation and EEG recording in RM1 of CAMKII-ARCHM1 mice. Right panel, fluorescent image showed restricted expression of ArchT-tdTomato in M1. Scale bar, 200 μm. b Representative spikes of M1 pyramidal neurons showing the reduced firing rate in response to yellow light stimulation. c Paradigms of yellow light stimulation in different phases in KA-induced seizures. d Effects of optogenetic inhibition of RM1 pyramidal neurons on the development of seizure stage during 90 min after KA injection. e–h Effects of different-phase optogenetic inhibition of RM1 pyramidal neurons on seizure stage (e), EEG onset (f), latency to GS (g) and number of GSs (h) in KA-induced seizures. i Representative EEGs and corresponding energy spectra of pyramidal neurons inhibition during seizure activity. j Schematic of viral injection (LM1), stimulation (LM1) and EEG recording (RM1) in CAMKII-ARCHM1 mice. k–n Effects of optogenetic inhibition of LM1 pyramidal neurons on seizure stage (k), EEG onset (l), latency to GS (m) and number of GSs (n) after KA injection. **p < 0.01, ***p < 0.001 and ****p < 0.001 compared with mCherry control group. Data shown as mean ± s.e.m. The number of mice used is indicated in figures. For detailed statistical information, see Supplementary Data 1. Source data are provided as a Source Data file.
