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Monoamines are implicated in a cognitive processes in a vari- ety of brain regions, including the hippocampal formation, where storage and retrieval of information are facilitated by synchronous network activ- ities. We have investigated the effects of norepinephrine, serotonin, and do- pamine on carbachol-, kainate-, and stimulus-induced hippocampal c-oscil- lations employing combined extra- and intracellular recordings. Mono- amines dose-dependently and reversibly suppressed kainate- and carbachol-induced c-oscillations while increasing the frequency. The effect of serotonin was mimicked by fenfluramine, which releases serotonin from presynaptic terminals. Forskolin also suppressed kainate- and carbachol- induced c-oscillations. This effect was mimicked by 8-Br-cAMP and isopro- terenol, an agonist of noradrenergic b-receptor suggesting that the mono- amines-mediated suppression of these oscillations could involve intracellu- lar cyclic adenosine 3 0 ,5 0 -cyclic monophosphate (AMP). By contrast, stimu- lus-induced c-oscillations were dose-dependently augmented in power and duration after monoamines application. Intracellular recordings from py- ramidal cells revealed that monoamines prolonged the stimulus-induced depolarization and membrane potential oscillations. Stimulus-induced c-oscillations were also suppressed by isoproterenol, the D1 agonist SKF-38393 forskolin, and 8-Br-cAMP. This suggests that the augmentation of stimulus-induced c-oscillations by monoamines involves—at least in part—different classes of cells than in case of carbachol- and kainate- induced c-oscillations. V C 2009 Wiley-Liss, Inc.

Hippocampal sharp wave-ripple complexes (SPW-Rs) occur during slow-wave sleep and behavioral immobility and are thought to represent stored information that is transferred to the neocortex during memory consolidation. Here we show that stimuli that induce long-term potentiation (LTP), a neurophysiological correlate of learning and memory, can lead to the generation of SPW-Rs in rat hippocampal slices. The induced SPW-Rs have properties that are identical to spontaneously generated SPW-Rs: they originate in CA3, propagate to CA1 and subiculum and require AMPA/kainate receptors. Their induction is dependent on NMDA receptors and involves changes in interactions between clusters of neurons in the CA3 network. Their expression is blocked by low-frequency stimulation but not by NMDA receptor antagonists. These data indicate that induction of LTP in the recurrent CA3 network may facilitate the generation of SPW-Rs.