Early memory formation disrupted by atypical PKC inhibitor ZIP in the medial prefrontal cortex but not hippocampus |
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| Authors: | Obaro Evuarherhe Gareth R.I. Barker Giorgia Savalli Elizabeth C. Warburton Malcolm W. Brown |
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| Affiliation: | 1. Department of Physiology and Pharmacology, University of Bristol, School of Medical Sciences, Bristol, United Kingdom;2. Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Vienna, Austria |
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| Abstract: | Atypical isoforms of protein kinase C (aPKCs; particularly protein kinase M zeta: PKMζ) 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 PKMζ pseudosubstrate peptide (ZIP) blocks PKMζ 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 PKCλ) in the mPFC during early memory formation. © 2014 Wiley Periodicals, Inc. |
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| Keywords: | recognition memory hippocampus medial prefrontal cortex encoding maintenance |
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