anti-apoptotic signaling system that regulates neuronal cell death during development and promotes survival in adult neurons (97, 98). The study by Sanna et al. expands our appreciation of normal physiologic roles for the PI-3-K pathway in mediating synaptic plasticity in the adult CNS. Their work suggests that PI3K activity is one of the processes necessary for the ongoing expression of LTP
expressed physiologically. This appears to be one aspect of an emerging picture. For example, Kelly and Lynch (99) have found that long-term potentiation in the dentate gyrus involves PI-3-K as well. Importantly, these studies point out the continuing recognition of the wide diversity of signal trans-duction mechanisms necessary for complex neuronal information processing.
BOX 3 (A) Inhibitors of PI3-kinase abate established LTP of fEPSP in the CA1 region. Synaptic potentials were simultaneously monitored in two independent pathways [white circles, stimulus 1 (S1); black squares, stimulus 2 (S2)]. An inhibitor of PI3-kinase, LY294002 (100 pM), was applied 30 minutes after delivery of HFS to one of the two pathways (S2). Insets are representative traces of extracellular fEPSPs recorded at the times marked by lowercase letters. Each representative trace is an average of five responses. Graphs represent the mean-normalized fEPSP slopes plotted against time. Arrows indicate when tetanic stimulation to one pathway (black squares) was given at time 0. A transient 20-minute application of LY294002 30 minutes after LTP induction abated LTP in the potentiated pathway (n = 7) (black squares), but no change was seen in the untetanized pathway (white circles). Data reproduced from Sanna et al. (96). Continued
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