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

AUTOR(ES)

Sacktor, T C

RESUMO

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.

Documentos Relacionados

• Rapid activation of hippocampal casein kinase II during long-term potentiation.
• Surface protein phosphorylation by ecto-protein kinase is required for the maintenance of hippocampal long-term potentiation.
• Synapse-specific protein kinase C activation enhances maintenance of long-term potentiation in rat hippocampus.
• Specificity of protein kinase inhibitor peptides and induction of long-term potentiation.
• Transient protein kinase C activation primes long-term depression and suppresses long-term potentiation of synaptic transmission in hippocampus.