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Arm immobilization causes cortical plastic changes and locally decreases sleep slow wave activity
TLDR
If a subject's arm is immobilized during the day, motor performance deteriorates and both somatosensory and motor evoked potentials decrease over contralateral sensorimotor cortex, indicative of local synaptic depression, suggesting cortical plasticity is linked to local sleep regulation without learning in the classical sense. Expand
Source modeling sleep slow waves
TLDR
High-density EEG (hd-EEG) source modeling is used to show that individual spontaneous slow waves have distinct cortical origins, propagate uniquely across the cortex, and involve unique subsets of cortical structures. Expand
Reduced sleep spindle activity in schizophrenia patients.
TLDR
The deficit in sleep spindles in schizophrenia subjects may reflect dysfunction in thalamic-reticular and thalamocortical mechanisms and could represent a biological marker of illness. Expand
Breakdown in cortical effective connectivity during midazolam-induced loss of consciousness
TLDR
It is found that, unlike during wakefulness, wherein TMS triggered responses in multiple cortical areas lasting for >300 ms, during midazolam-induced LOC, TMS-evoked activity was local and of shorter duration, and a measure of the propagation of evoked cortical currents could reliably discriminate between consciousness and LOC. Expand
Sleep homeostasis and cortical synchronization: III. A high-density EEG study of sleep slow waves in humans.
TLDR
In the human EEG, the decline of SWA during sleep is accompanied by changes in slow-wave parameters that were predicted by a computer model simulating a homeostatic reduction of cortical synaptic strength. Expand
Propofol anesthesia and sleep: a high-density EEG study.
TLDR
Propofol anesthesia is a sleep-like state and slow waves are associated with diminished consciousness even in the presence of high gamma activity. Expand
Thalamic dysfunction in schizophrenia suggested by whole-night deficits in slow and fast spindles.
TLDR
Results indicate that spindle deficits can be reliably established in schizophrenia, are stable across the night, are unlikely to be due to antipsychotic medications, and point to deficits in the thalamic reticular nucleus and thalamo-reticular circuits. Expand
Triggering sleep slow waves by transcranial magnetic stimulation
TLDR
TMS triggering of slow waves reveals intrinsic bistability in thalamocortical networks during non-rapid eye movement sleep and leads to a deepening of sleep and to an increase in EEG slow-wave activity, which is thought to play a role in brain restoration and memory consolidation. Expand
The neural correlates of dreaming
TLDR
Monitoring this posterior 'hot zone' in real time predicted whether an individual reported dreaming or the absence of dream experiences during NREM sleep, suggesting that it may constitute a core correlate of conscious experiences in sleep. Expand
Concomitant BDNF and sleep slow wave changes indicate ketamine-induced plasticity in major depressive disorder.
TLDR
Findings suggest that higher SWA and BDNF levels may respectively represent electrophysiological and molecular correlates of mood improvement following ketamine treatment, and enhanced synaptic plasticity - as reflected by increased SWA, individual slow wave parameters and plasma BDNF - is part of the physiological mechanism underlying the rapid antidepressant effects of NMDA antagonists. Expand
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