Early memory formation disrupted by atypical PKC inhibitor ZIP in the medial prefrontal cortex but not hippocampus

Obaro Evuarherhe, Gareth Barker, Giorgia Savalli, Clea Warburton, Malcolm Brown

Research output: Contribution to journalArticle (Academic Journal)peer-review

18 Citations (Scopus)

Abstract

Atypical isoforms of protein kinase C (aPKCs; particularly protein kinase M zeta: PKM zeta) have been hypothesized to be necessary and sufficient for the maintenance of long-term potentiation (LTP) and long term memory by maintaining postsynaptic AMPA receptors via the GluA2 subunit. A myristoylated PKM zeta pseudosubstrate peptide (ZIP) blocks PKM zeta activity. We examined the actions of ZIP in medial prefrontal cortex (mPFC) and hippocampus in associative recognition memory in rats during early memory formation and memory maintenance. ZIP infusion in either hippocampus or mPFC impaired memory maintenance. However, early memory formation was impaired by ZIP in mPFC but not hippocampus; and blocking GluA2-dependent removal of AMPA receptors did not affect this impairment caused by ZIP in the mPFC. The findings indicate: (i) a difference in the actions of ZIP in hippocampus and medial prefrontal cortex, and (ii) a GluA2-independent target of ZIP (possibly PKC lambda) in the mPFC during early memory formation.
Original languageEnglish
Pages (from-to)934-942
Number of pages9
JournalHippocampus
Volume24
Issue number8
DOIs
Publication statusPublished - Aug 2014

Keywords

  • recognition memory
  • Hippocampus
  • medial prefrontal cortex
  • encoding
  • Maintenance

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