This inhibitory effect was demonstrated by a decrease in the percentage of bursting neurons (OGD/R: 66.7%, 16 out of 24; OGD/ R + K252a: 18.2%, 2 out of 11, p < 0.01, Figure 6B ), a decrease in bursting frequency ( F (2,50) = 9.04, OGD/R: 0.014 ± 0.015 Hz, n = 24; OGD/ R + K252a: 0.002 ± 0.004 Hz, n = 11, p = 0.006, Figure 6C ), and a decreasing trend in the total number of APs ( F (2,50) = 5.36, OGD/R: 166.8 ± 221.9, n = 24 vs.
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KCC2 Dysfunction Mediated by Microglial BDNF/TrkB Signaling Exacerbates Early Post-Stroke Seizure Susceptibility.
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When the BDNF/TrkB signaling pathway was blocked with K252a, mIPSCs showed a trend toward increased amplitude ( F (2,47) = 5.79, MCAO‐R: 17.0 ± 3.4 pA, N = 3, n = 17 vs.