Persistent activation of the zeta isoform of protein kinase C in the maintenance of long-term potentiation.

TLDR

Long‑term potentiation in hippocampal CA1 consists of an induction phase followed by a maintenance phase, and protein kinase C isoforms are thought to contribute to both stages. In CA1 slices, PKC isoforms rapidly translocate to the particulate fraction after tetanus but this shift does not persist, whereas PKMζ accumulates in the cytosol during maintenance, indicating a switch from PKC translocation to PKMζ formation underlies LTP induction and maintenance.

Abstract

Long-term potentiation in the CA1 region of the hippocampus, a model for memory formation in the brain, is divided into two phases. A transient process (induction) is initiated, which then generates a persistent mechanism (maintenance) for enhancing synaptic strength. Protein kinase C (PKC), a gene family of multiple isozymes, may play a role in both induction and maintenance. In region CA1 from rat hippocampal slices, most of the isozymes of PKC translocated to the particulate fraction 15 sec after a tetanus. The increase of PKC in the particulate fraction did not persist into the maintenance phase of long-term potentiation. In contrast, a constitutively active kinase, PKM, a form specific to a single isozyme (zeta), increased in the cytosol during the maintenance phase. The transition from translocation of PKC to formation of PKM may help to explain the molecular mechanisms of induction and maintenance of long-term potentiation.