Sacktor T C, Osten P, Valsamis H, Jiang X, Naik M U, Sublette E
Department of Pharmacology, State University of New York at Brooklyn 11203.
Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8342-6. doi: 10.1073/pnas.90.18.8342.
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.
海马体CA1区的长时程增强是大脑中记忆形成的一个模型,它分为两个阶段。一个短暂的过程(诱导)开始,随后产生一种持久的机制(维持)来增强突触强度。蛋白激酶C(PKC)是一个具有多种同工酶的基因家族,可能在诱导和维持过程中都发挥作用。在大鼠海马切片的CA1区,破伤风后15秒,大多数PKC同工酶转移到颗粒部分。颗粒部分中PKC的增加并没有持续到长时程增强的维持阶段。相比之下,一种组成型活性激酶PKM,是单一同工酶(ζ)特有的形式,在维持阶段胞质溶胶中增加。从PKC易位到PKM形成的转变可能有助于解释长时程增强诱导和维持的分子机制。