This is page is an unedited draft from Marcello’s manuscript. It needs citations, figures, cross-links, and other work to be done. It will take a while!
It is here so you can see the general gist of Marcello’s argument across the whole essay.
Feel free to visit from time to time for updates.
The alternation of sleep with awake states is controlled be sleep-promoting and wake-promoting neurons, indicating that sleep is an active process modulated by daily cycle of light and sensory inputs. The phases of sleep, initially deduced from low spatial resolution EEG, led to the distinction between rapid eye movement (REM) sleep and non-REM (NREM) sleep, also called deep sleep. Deep sleep involves a physiological transient loss of consciousness and is associated with a significant disconnection from sensory inputs and is characterised by brain waves of low frequency1.
Blood flow oscillations associated with sleep measured via fMRI have distinct spatiotemporal patterns across the brain, suggesting that some regions enter a sleeping state earlier than others. For instance, the thalamus was the first region to show sleep-associated blood flow patterns, consistent with EEG data2.
In deep NREM sleep, thalamo-cortical neurons show slow (<1 Hz) oscillations comprising recurring changes in membrane potentials described as UP and DOWN states. During slow-wave sleep, the cells become hyperpolarised and thus often burst rhythmically, which reduces relay of information to cortex.
Travelling waves in the human cortex since have been observed by EEG at the whole-brain scale. At larger spatial scales, the orderly slow-wave propagation dominates; at the finer scale non-REM sleep is characterised by more complex propagation patterns3. During deep sleep, slow waves travel from the frontal cortex to the occipital lobes4.
Slow waves also occur in cats and are also evident in thalamic nuclei (ventro-basal complex, medial geniculate body; ventral lateral nucleus) and two thalamic nuclei in rats and mice (lateral geniculate nucleus and ventro-basal complex). These groups of neurons share several basic properties including, the stereotypical, rhythmic alternation between distinct UP and DOWN states.
Some neurons in the thalamus isolated from the cortex also behave as pacemakers with similar biophysical properties. Thus, the thalamus might also play an active role in shaping cortical slow wave activity.
During deep sleep brain waves of higher frequencies, called spindles, also occur. These consist in 11–15 Hz oscillations lasting 0.5–2.0 s that persist for ~6–15 cycles.
Oscillations at 4-8 Hz (theta waves) previously thought to be approximately synchronous throughout the cortex of the hippocampus, are in fact travelling waves.
- AR Adamantidis et al (2019): Oscillating circuitries in the sleeping brain. Nature Reviews Neuroscience 20, 746-762. ↩︎
- C Song et al (2022): fMRI spectral signatures of sleep. Proceedings of the National Academy of Sciences USA 119, e2016732119. ↩︎
- B Hangya et al (2011): Complex propagation patterns characterize human cortical activity during slow-wave sleep. Journal of Neuroscience 31, 8770–8779;
L Muller et al (2018): Cortical travelling waves: mechanisms and computational principles. Nature Reviews Neuroscience 19,255–268. ↩︎ - M Massimini et al (2004): The sleep slow oscillation as a traveling wave. Journal of Neuroscience 24, 6862–6870.
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