Fig. 9.

Postsynaptically applied phalloidin reduces the maintenance of pairing-induced LTP. Gray bar indicates the period of internal perfusion of phalloidin or DMSO, andthick arrow indicates pairing. Error bars indicate SEM.A, In control (n = 8), 0.1% DMSO was applied 2 min after LTP induction by pairing (filled rectangles). The average EPSCs in the LTP and in the non-LTP pathway (open rectangles) measured 2 min after pairing were 330 and 81% of the baseline. The average EPSCs in the LTP path and in the non-LTP path measured at 50 min after induction were 407 and 114% of the baseline, which gave 357% of relative potentiation.B, Phalloidin (100 μm) was perfused 2 min after pairing (n = 9). The average EPSCs in the LTP path (filled circles) and in the non-LTP path (open circles) measured at 2 min after induction were 311 and 74% of the baseline. The average EPSCs in the LTP path and in the non-LTP path measured at 50 min after induction were 134 and 49% of the baseline, which gave 273% of relative potentiation. Therefore, phalloidin application reduced the potentiation of LTP by 33% at 50 min after induction. Bottom panelshows the input resistance as a function of time. C, Ratio of average EPSC in the LTP path over that in the non-LTP path as a function of time. The ratio was normalized to the ratio at 2 min after induction. The larger decay in the ratio was produced by phalloidin (filled circles; n= 9; from B) compared with that with DMSO control (open circles; n = 8; fromA), which indicates a more selective effect of phalloidin on LTP maintenance. Cumulative distribution of the ratio of EPSC in the LTP path to that in the non-LTP path measured at 30 min after LTP induction (asterisks inA and B). The ratio from phalloidin experiment (filled circles; n= 8) was significantly shifted from that from control DMSO experiment (open circles; n = 8), indicating a significant reduction in LTP at 30 min after induction by postsynaptic phalloidin (K–S test; Q ≪ 0.01).