@article{Sanna01052002,
author = {Sanna, Pietro Paolo and Cammalleri, Maurizio and Berton, Fulvia and Simpson, Cindy and Lutjens, Robert and Bloom, Floyd E. and Francesconi, Walter}, 
title = {Phosphatidylinositol 3-Kinase Is Required for the Expression But Not for the Induction or the Maintenance of Long-Term Potentiation in the Hippocampal CA1 Region},
volume = {22}, 
number = {9}, 
pages = {3359-3365}, 
year = {2002}, 
doi = {10.1523/JNEUROSCI.22-09-03359.2002}, 
abstract ={Several signal transduction pathways have been implicated in the induction of long-term potentiation (LTP), yet the signal transduction mechanisms behind the maintenance–expression phase of LTP are still poorly understood. We investigated the role of phosphatidylinositol 3-kinase (PI3-kinase) in LTP at Schaffer collateral/commissural fiber–CA1 synapses in rat hippocampal slices using biochemical approaches and extracellular electrophysiological recordings. We observed that PI3-kinase activity was induced in the CA1 region during LTP of field EPSPs (fEPSPs) and that two structurally unrelated PI3-kinase inhibitors, LY294002 and wortmannin, abated established LTP, suggesting that PI3-kinase is involved in the maintenance–expression phase of LTP. However, LTP recovered after washout of the reversible PI3-kinase inhibitor LY294002, confirming that LTP maintenance and expression are distinct events and indicating that PI3-kinase activity is required for LTP expression rather than for its maintenance. Interestingly, preincubation with LY294002 did not prevent LTP induction. In fact, if LY294002 was withdrawn 5 min after high-frequency stimulation, an LTP of fEPSP was seen. Last, a voltage-dependent calcium channel-dependent form of LTP in the CA1 could also be reversibly abated by LY294002, raising the possibility that PI3-kinase could be required for the expression of multiple forms of synaptic potentiation.}, 
URL = {http://www.jneurosci.org/content/22/9/3359.abstract}, 
eprint = {http://www.jneurosci.org/content/22/9/3359.full.pdf+html}, 
journal = {The Journal of Neuroscience} 
}