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. 2013 Oct 30;33(44):17290–17300. doi: 10.1523/JNEUROSCI.2619-13.2013

Figure 9.

Figure 9.

SGE-201 and SGE-301 reverse synaptic plasticity deficits following NMDA receptor blockade. A, B, Reversal of ketamine suppression of long-term potentiation (LTP) by 24(S)-HC (A) and SGE-201 (B) in P30 hippocampal slices. Open symbols are baseline response following ketamine administration (1 μm, 30 min preincubation) to 100 Hz × 1 s HFS (vertical arrow). The change in baseline EPSP slope was 93.1 ± 2.3% 60 min following HFS in ketamine-treated control slices. Solid symbols represent the same condition except 0.5 μm 24(S)-HC (A; 131.3 ± 6.7% of baseline, p < 0.001, N = 5) or SGE-201 (B; 129.1 ± 9.2% of baseline, p < 0.001, N = 5) was present; N = 5 each, p = 0.008. Calibration bars: 1 mV, 5 ms.