The remarkable mechanism of prostaglandin E2 on synaptic plasticity.

Prostanoids have a broad spectrum of biological activities in a variety of organs including the brain. However, their effects on synaptic plasticity in the brain, which have been recently revealed, are ambiguous in comparison to those in the other organs. Prostaglandin E(2) (PGE(2)) is a prostanoid produced from arachidonic acid in the cellular membrane, and knowledge about its functions is increasing. Recently, a novel function of PGE(2) in the brain has shed light on aspects of synaptic plasticity such as long-term potentiation (LTP). More recently, we have proposed a hypothesis for the mechanisms of this PGE(2)-related form of synaptic plasticity in the visual cortex. This involves the dynamics of two subtypes of PGE(2) receptors that have opposing functions in intracellular signal transduction. Consequently, mechanisms that increase the level of cyclic AMP in the cytosol may explain for the mechanisms of LTP in the visual cortex. The current notion of bidirectional trafficking of PGE(2) receptors under this hypothesis is reminiscent of the "silent synapse" mechanism of LTP on the trafficking of the AMPA receptors between the membrane and cytosol. Moreover, we propose the hypothesis that PGE(2) acts as a "post-to-postsynaptic messenger" for the induction of LTP in the visual cortex. This review describes a complex mode of action of PGE(2) receptors in synaptic plasticity in the brain.