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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: Neuropharmacology. 2016 Feb 8;105:378–387. doi: 10.1016/j.neuropharm.2016.02.008

Fig. 3. Nicotine-induced depotentiation was not accompanied by dephosphorylation of Ser-831 on GluA1 of AMPARs.

Fig. 3

A. LTP induction increased the level of Ser-831 phosphorylation. Western blot analysis with anti-GluA1 phospho Ser-831 antibody and anti-GluA1 antibody was carried out with protein samples from CA1 slices, which received baseline stimulation only (BL) or in which LTP was induced (LTP). Representative phospho-Ser-831 (P-S831) and GluA1 bands are shown (top). Phosphorylation at Ser-831 was analyzed by normalizing the signal from phosphorylation site-specific antibody to the total amount of GluA1 measured using anti-GluA1 antibody. Summary data are presented (bottom). B. LFS delivered to potentiated slices did not alter the level of Ser-831 phosphorylation. Protein samples from LTP slices (LTP) and LFS delivered-LTP slices (LFS) are compared. C. Nicotine-induced depotentiation did not change the level of Ser-831 phosphorylation. LFS was delivered to slices in the absence or presence of nicotine after LTP induction. Protein samples from LFS alone slices (LFS) and LFS + nicotine slices (Nic-DP) are compared. **P<0.01.