Geon The Maintenance of LTP by PKMζ Papers



This paper reviews evidence for the role of PKMζ in maintaining long-term potentiation (LTP) and discusses whether or not the long-lasting memory (> 1 month) is stored in PKMζ. The LTP induction may cause protein kinase A (PKA) to translocate from spines to the nucleus, triggering expression of the brain-derived neurotrophic factor (BDNF), which subsequently induces production of plasticity-related proteins, including PKMζ - a persistently active atypical protein kinase C (aPKC). Once synthesized near the synapse, the active PKMζ may up-regulate the GluA2-containing AMPA receptors (AMPARs) to maintain LTP. On the other hand, the translation of PKMζ is negatively regulated by the α-subunit of eukaryotic initiation factor 2 (eIF2α), which in turn is controlled by protein kinase-like ER kinase (PERK). PKMζ was thought to store lifelong memories based on the finding that its inhibitor, zeta inhibitory peptide (ZIP), abolished the memory of conditioned taste aversion even 3 mo after encoding, but a recent study demonstrated that ZIP had no effect if applied two weeks or one month later. According to the Synaptogenesis Hypothesis presented in this paper, PKMζ should become dispensable after consolidation is complete.


Read Online Download PDF


Old PDF Version