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See detailCerebral asymmetries in sleep-dependent processes of memory consolidation
Peigneux, Philippe ULg; Schmitz, Remy; Willems, Sylvie ULg

in Learning & Memory (2007), 14(6), 400-406

Preference for previously seen, unfamiliar objects reflects a memory bias on affective judgment, known as the "mere exposure effect" (MEE). Here, we investigated the effect of time, post-exposure sleep ... [more ▼]

Preference for previously seen, unfamiliar objects reflects a memory bias on affective judgment, known as the "mere exposure effect" (MEE). Here, we investigated the effect of time, post-exposure sleep, and the brain hemisphere solicited on preference generalization toward objects viewed in different perspectives. When presented in the right visual field (RVF), which promotes preferential processing in the left hemisphere, same and mirrored exemplars were preferred immediately after exposure. MEE generalized to much dissimilar views after three nights of sleep. Conversely, object presentation in the left visual field (LVF), promoting right hemisphere processing, elicited a MEE for same views immediately after exposure, then for mirror views after sleep. Most importantly, sleep deprivation during the first post-exposure night, although followed by two recovery nights, extinguished MEE for all views in the LVF but not in the RVF. Besides demonstrating that post-exposure time and sleep facilitate the generalization process by which we integrate various representations of an object, our results suggest that mostly in the right hemisphere, sleep may be mandatory to consolidate the memory bias underlying affective preference. These interhemispheric differences tentatively call for a reappraisal of the role of cerebral asymmetries in wake- and sleep-dependent processes of memory consolidation. [less ▲]

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See detailMetaplastic effect of apamin on LTP and paired-pulse facilitation
Ris, L.; Capron, B.; Sclavons, C. et al

in Learning & Memory (2007), 14(6), 390-399

In area CA1 of hippocampal slices, a single 1-sec train of 100-Hz stimulation generally triggers a short-lasting long-term potentiation (S-LTP) of 1-2 h. Here, we found that when such a train was applied ... [more ▼]

In area CA1 of hippocampal slices, a single 1-sec train of 100-Hz stimulation generally triggers a short-lasting long-term potentiation (S-LTP) of 1-2 h. Here, we found that when such a train was applied 45 min after application of the small conductance Ca2+-activated K+ (SK) channel blocker apamin, it induced a long-lasting LTP (L-LTP) of several hours, instead of an S-LTP. Apamin-induced SK channel blockage is known to resist washing. Nevertheless, the aforementioned effect is not a mere delayed effect; it is metaplastic. Indeed, when a single train was delivered to the Schaffer's collaterals during apamin application, it induced an S-LTP, like in the control situation. At the moment of this LTP induction (15th min of apamin application), the SK channel blockage was nevertheless complete. Indeed, at that time, under the influence of apamin, the amplitude of the series of field excitatory postsynaptic potentials (fEPSPs) triggered by a stimulation train was increased. We found that the metaplastic effect of apamin on LTP was crucially dependent on the NO-synthase pathway, whereas the efficacy of the NMDA receptors was not modified at the time of its occurrence. We also found that apamin produced an increase in paired-pulse facilitation not during, but after, the application of the drug. Finally, we found that the induction of each of these two metaplastic phenomena was mediated by NMDA receptors. A speculative unitary hypothesis to explain these phenomena is proposed. [less ▲]

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