N-Cadherin Regulates Cytoskeletally Associated IQGAP1/ERK Signaling and Memory Formation

Christina Schrick, Andre Fischer, Deepak P. Srivastava, Natalie C. Tronson, Peter Penzes, Jelena Radulovic

Research output: Contribution to journalArticlepeer-review

84 Scopus citations


Cadherin-mediated interactions are integral to synapse formation and potentiation. Here we show that N-cadherin is required for memory formation and regulation of a subset of underlying biochemical processes. N-cadherin antagonistic peptide containing the His-Ala-Val motif (HAV-N) transiently disrupted hippocampal N-cadherin dimerization and impaired the formation of long-term contextual fear memory while sparing short-term memory, retrieval, and extinction. HAV-N impaired the learning-induced phosphorylation of a distinctive, cytoskeletally associated fraction of hippocampal Erk-1/2 and altered the distribution of IQGAP1, a scaffold protein linking cadherin-mediated cell adhesion to the cytoskeleton. This effect was accompanied by reduction of N-cadherin/IQGAP1/Erk-2 interactions. Similarly, in primary neuronal cultures, HAV-N prevented NMDA-induced dendritic Erk-1/2 phosphorylation and caused relocation of IQGAP1 from dendritic spines into the shafts. The data suggest that the newly identified role of hippocampal N-cadherin in memory consolidation may be mediated, at least in part, by cytoskeletal IQGAP1/Erk signaling.

Original languageEnglish (US)
Pages (from-to)786-798
Number of pages13
Issue number5
StatePublished - Sep 6 2007
Externally publishedYes



ASJC Scopus subject areas

  • General Neuroscience


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