Summary Long-term plasticity contributes to memory formation and sleep plays a critical role in memory consolidation. However, it is unclear whether sleep slow oscillation by itself induces long-term plasticity that contributes to memory retention. Using in vivo pre-thalamic electrical stimulation at 1 Hz which itself does not induce immediate potentiation of evoked responses, we investigated how the cortical evoked response was modulated by different states of vigilance. We found that somatosensory evoked potentials during wake were enhanced after a slow-wave sleep episode (with or without stimulation during sleep) as compared to a previous wake episode. In vitro, we determined that this enhancement has a postsynaptic mechanism that is calcium-dependent, requires hyperpolarization periods (slow waves), and requires a co-activation of both AMPA and NMDA receptors. Our results suggest that long-term potentiation occurs during slow-wave sleep supporting its contribution to memory.

Sleep plays a key role in multiple cognitive functions and sleep pattern changes with aging. Human studies revealed that aging decreases sleep efficiency and reduces the total sleep time, the time spent in slow-wave sleep (SWS), and the delta power (1–4 Hz) during sleep; however, some studies of sleep and aging in mice reported opposing results. The aim of our work is to estimate how features of sleep–wake state in mice during aging could correspond to age-dependent changes observed in human. In this study, we investigated the sleep/wake cycle in young (3 months old) and older (12 months old) C57BL/6 mice using local-field potentials (LFPs). We found that older adult mice sleep more than young ones but only during the dark phase of sleep-wake cycle. Sleep fragmentation and sleep during the active phase (dark phase of cycle), homologous to naps, were higher in older mice. Older mice show a higher delta power in frontal cortex, which was accompanied with similar trend for age differences in slow wave density. We also investigated regional specificity of sleep–wake electrographic activities and found that globally posterior regions of the cortex show more rapid eye movement (REM) sleep whereas somatosensory cortex displays more often SWS patterns. Our results indicate that the effects of aging on the sleep–wake activities in mice occur mainly during the dark phase and the electrode location strongly influence the state detection. Despite some differences in sleep–wake cycle during aging between human and mice, some features of mice sleep share similarity with human sleep during aging.

Neuronal synchronization can be defined as a correlated appearance in time of two or more events associated with various aspects of neuronal activity. Neuronal synchronization depends on chemical and electrical synaptic as well as ephaptic and non-specific interactions. We consider two distinct types of neuronal synchronization: local synchronization that is responsible for the generation of local field potentials; and long-range synchronization, detected with distantly located electrodes and mediated primarily via chemical synaptic interactions, which contributes to the EEG synchronization. Neocortical synchronization during sleep and wakefulness is often associated with rhythmic oscillations of neuronal activity: slow oscillation, delta, spindle, beta, gamma and ripples. Normal thalamocortical oscillations [sleep or wake oscillations] are generated as a result of both local and long-range synchronization. During paroxysmal [seizure] activity, the role of chemical synaptic interactions decreases because of alterations in ionic composition that impairs synaptic transmission. Synchronized activities in large population of neurons (such as neocortex) may occur as nearly simultaneous patterns across an entire population or as propagating waves. Neocortical synchronization is controlled by the activities in ascending systems: cholinergic, norepinephrinergic and serotoninergic. The presence of cortico-thalamo-cortical feedback loops contribute to the synchronization of cortical activities. We propose that all the types of neuronal interactions contribute to the generation of synchronous oscillatory activities, but the ratio of their contribution is different for different types of oscillations.Neuronal synchronization can be distinguished into long-range and local synchronization. The long-range synchrony is usually detected with two or more electrodes placed at some distance apart. It leads to brain activity that is correlated at long distances and may be seen using both local filed potential (LFP) and electroencephalogram (EEG) recordings. The first tool (i.e., the LFP) provides a microscopic measure of brain activity summarizing electrical activities of possibly thousands of neurons 1-4 . The second type of recording (i.e., the EEG) is a result of changes of electrical activity of multiple sources and ultimately represents activity patterns of large populations of neurons and glial cells in the brain. The local or short-range synchrony †Correspondence should be sent to: Igor Timofeev,

The neocortex is the site of origin of several forms of acquired epilepsy. Here we provide a brief review of experimental models that were recently developed to study neocortical epileptogenesis as well as some major results obtained with these methods. Most of neocortical seizures appear to be nocturnal and it is known that neuronal activities reveal high levels of synchrony during slow-wave sleep. Therefore, we start the review with a description of mechanisms of neuronal synchronization and major forms of synchronized normal and pathological activities. Then, we describe three experimental models of seizures and epileptogenesis: ketamine-xylazine anesthesia as feline seizure triggered factor, cortical undercut as cortical penetrating wound model and neocortical kindling. Besides specific technical details describing these models we also provide major features of pathological brain activities recorded during epileptogenesis and seizures. The most common feature of all models of neocortical epileptogenesis is the increased duration of network silent states that up-regulates neuronal excitability and eventually leads to epilepsy.