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. Author manuscript; available in PMC: 2009 Jun 1.
Published in final edited form as: Mol Cell Neurosci. 2008 Mar 18;38(2):236–244. doi: 10.1016/j.mcn.2008.02.013

Figure 5.

Figure 5

EphrinB1 enhancement of α7-nAChR-induced long-lasting pCREB. E14 CG neurons were treated with Fc/Ab (Con) or ephrinB1-Fc/Ab (Ephrin) and the indicated compounds followed by 10 μM nicotine (Nic) for 5 min in the presence of 200 μM cadmium to block voltage-gated calcium channels, and then incubated an additional 20 min in the absence of nicotine before fixing, staining, and immunostaining for nuclear pCREB. Values represent the mean ± SEM for the proportion of labeled cells. Asterisk, p < 0.05; double asterisk, p < 0.01; multi-line comparisons: group members compared to “No Blkr”. EhprinB1 treatment increased the proportion of cells showing long-term pCREB, and the increase was entirely attributable to α7-nAChRs (blocked by αBgt) and dependent on a tyrosine receptor kinase (blocked by K252a), a Src family member (blocked by SU6656; also blocked by PP2 but not PP3, not shown), PI3 kinase (blocked by LY294002) and PKA (blocked by KT5720) but not on calcium release from internal stores (not blocked by thapsigargin).