Figure 2.

Enhanced LTP in S100B-null mice. (A) Two consecutive stimulations were applied at various interpulse intervals. Paired pulse facilitation did not differ between wild-type (n = 6 slices/3 mice, closed circles) and mutant mouse slices (n = 6 slices/3 mice, open circles). (B) The averaged time course of LTP in wild-type (n = 13 slices/7 mice) and mutant (n = 13 slices/7 mice) mouse slices are shown. Tetanic stimulation was applied at time points 0 and 30 min, as indicated by the arrows. The representative traces, 1, 2, and 3, were taken from the time points 0, 30, and 50 min, respectively. (C) The NMDA receptor antagonist D-APV (50 μM) was applied during the time period indicated. D-APV completely prevented the second LTP in both wild-type (n = 9 slices/5 mice) and mutant (n = 9 slices/5 mice) mouse slices. (D) The mutant mouse slices (n = 9 slices/5 mice) had significantly greater potentiation than the wild-type mouse slices (n = 8 slices/5mice) in the presence of the GABA_A receptor blocker picrotoxin (50 μM). (E) Saturated LTP was induced by five tetanic stimulations at 10-min intervals. Mutant mouse slices (n = 12 slices/5 mice) had significantly greater potentiation than wild-type mouse slices (n = 12 slices/5mice) at the saturated state. Data represent mean ± SE.