This indicates that waking period can increase the excitability of callosal axons. (2) The frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs) Autophagy inhibitor purchase are higher in slices collected from animals after prolonged waking as compared to sleep (Liu et al., 2010). This is likely due to a rebound over excitability in the absence of acetylcholine. Indeed, waking state is characterized by activities of the cholinergic system and acetylcholine reduces the amplitude of excitatory postsynaptic potentials (EPSPs) (Gil et al., 1997; Figure 5D). (3) In somatosensory cortical slices of juvenile rats, calcium-permeable

AMPA receptors were shown to be present at the synapse when animals were sacrificed after the wake period and they were absent after the sleep period (Lanté et al., 2011). Obviously, not all types of AMPA receptors are removed from synapses during sleep; thus, it does not preclude the insertion of other AMPA receptor types at synapses during sleep. A recent study in cats showed that intracortical inhibition of mTOR signaling abolished sleep-dependent plasticity, while no effects were observed in the plasticity induced during wake (Seibt et al., 2012). Therefore, it is very likely that plasticity CT99021 induced during wake or during sleep has different mechanisms. The stimulation of medial lemniscal

fibers is not a learning task per se; thus, it is difficult to affirm whether this experiment simulates a declarative or a nondeclarative learning task. However, most procedural learning tasks implicate the somatosensory system and procedural memory was shown to benefit from SWS (Huber et al., 2004; Rasch et al., 2009), which is also in agreement with our results. The enhancement

of responses was always present after the first SWS episode and often also after the second SWS episode, but then the response was saturated. Our results suggest that, once potentiated, the response cannot be further potentiated for a certain time window. next This is in agreement with studies on humans showing that mainly early sleep and naps, rich in slow waves, are important for memory improvement (Gais et al., 2000; Mednick et al., 2003; Nishida and Walker, 2007). Our results show a potentiation of cortical responsiveness after a period of SWS and that an imitation of sleep slow oscillation in vitro was sufficient to strengthen the cortical synapses, providing a physiological mechanism for sleep-dependent memory formation. Experiments were carried out in accordance with the guideline of the Canadian Council on Animal Care and approved by the Laval University Committee on Ethics and Animal Research. Experiments were conducted on four adult nonanesthetized cats. The cats were purchased from an established animal breeding supplier.