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. 2000 Mar 21;97(8):4315–4320. doi: 10.1073/pnas.070022697

Figure 1.

Figure 1

BDNF restores LTP in PSA-NCAM-deficient slices. (A) Induction of LTP using TBS in slices prepared from NCAM-deficient mice resulted in a decaying potentiation (●, TBS1). However, restimulation of the same pathway (●, TBS2) or of another independent, naive input (○, TBS2) after BDNF application (100 ng/ml, bar) restored LTP. Data are mean ± SEM of five experiments. (B) LTP induction in slice cultures treated with Endo-N, an enzyme that selectively cleaves the PSA moiety of NCAM. The defective LTP observed in Endo-N treated cultures (TBS1) was restored when stimulation was reapplied after BDNF application (100 ng/ml, TBS2). Data are mean ± SEM of four experiments. (C) The LTP induced by TBS in the presence of BDNF in NCAM-deficient slices remained stable for over 1 h. Data are mean ± SEM of 3–4 experiments. (D) Summary of the amount of LTP induced by TBS in the various conditions tested: slices of wild-type mice (WT, n = 3–6) and NCAM knockout mice recorded in the absence (NCAM −/−) or presence of BDNF (100 ng/ml, n = 7–10); nontreated organotypic slice cultures (n = 6), slice cultures treated for 12 h with Endo-N (n = 6), and slice cultures treated for 12 h with Endo-N but exposed for 30 min to 100 ng/ml BDNF (n = 7). The defective LTP observed in NCAM knockout mice and Endo-N-treated cultures is fully restored by BDNF.