Pi3kinase And Eltp Expression

Sanna et al. recently reported that the activity of the PI-3-Kinase cascade is necessary for the expression of E-LTP in area CA1 (96). The essence of their findings is that PI-3-K and its target AKT are activated in E-LTP, and that PI-3-K inhibitors like LY294002 can block the expression of LTP (see Panel A). While the upstream regulators and downstream tarets of this cascade in E-LTP are mysterious at present, this finding represents an opportunity to introduce the basics of the PI-3-K cascade in the context of synaptic plasticity in area CA1.

PI-3-K is phosphatidylinositol-3-kinase, which synthesizes polyphosphoinositides

(e.g., PIP3) in the plasma membrane. One of its principal targets is AKT (named for the transforming AKT8 retrovirus strain and also known as protein kinase B). By and large, this pathway has the attribute that it does not utilize readily diffusible second messengers, but rather relies on multiprotein signaling complexes and the translocation of activated proteins to various subcellular locales in order to achieve its effects. PI-3-K itself phosphorylates inositol-containing phospholipids, which subsequently activate AKT by binding to its pleckstrin homology (PH) domain (see Panel B).

To date, most work on PI-3-K/AKT in neurons has focused on its role as an

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