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. Author manuscript; available in PMC: 2009 Oct 28.
Published in final edited form as: Neuroscience. 2008 Aug 27;156(4):872–884. doi: 10.1016/j.neuroscience.2008.08.042

Fig. 6.

Fig. 6

Evidence that PKCζ is upstream from and actives p-ERK during in vitro conditoning. (A) ZIP applied for two pairing sessions (ZIP2) at the beginning of conditioning suppresses expression of p-PKCζ/λ to pseudoconditioned levels compared to conditioning. (B) Application of ZIP also suppresses p-ERK expression, while the PKC antagonist Che does not. (C) The ERK and p38 MAPK antagonists PD98059 (PD) and SB203580 (SB), respectively, fail to affect levels of p-PKCζ/λ compared to conditioning. (D) Coimmunoprecipitation experiments reveal that t-PKCζ, p-PKCζ/λ, and PKMζ interact with t-ERK while t-PKC does not. * indicate significant differences from Ps. P values are given in the text.