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. 1997 Oct 14;94(21):11675–11680. doi: 10.1073/pnas.94.21.11675

Figure 3.

Figure 3

(A) Mean number of X-Gal-stained cells in the ipsilateral side of the 2- and 3-day LTP group animals with GAP-43 PATE in the inner molecular layer (IML; n = 7) in CHR or in IHR compared with the number of stained cells on the contralateral side. Error bars represent SEM. ∗, P < 0.05; one-way ANOVA. In the group sacrificed 1 day after LTP induction, 1 of 5 animals showed transgene induction in the IML. In animals sacrificed 2 and 3 days after LTP induction, 7 of 10 showed β-galactosidase in the inner molecular layer, whereas only 1 of 12 LFC and unoperated animals showed expression in that same region (P < 0.05; χ2 analysis). (B) Hypothetical scheme to indicate (i) the origin of the X-Gal-staining band induced by LTP in the inner molecular layer bilaterally and (ii) potential growth of mossy cell (MC) axon terminals. Two to three days after LTP induction, GAP-43 PATE in mossy cells leads to bilateral axonal transport of β-galactosidase. Specifically, tetanic stimulation of perforant path (I) induces potentiated responses in granule cells (GC). After receiving excitatory synaptic input from granule cells (II), transgene and endogenous GAP-43 mRNA expression (III) is induced in MC. β-Galactosidase induced in MC is transported bilaterally into the axonal terminal region in the inner molecular layer (IV). Arborization of axonal terminals (V) after LTP increases GAP-43 expression in the mossy cells is proposed.