Why Non-rapid Eye Movement (NREM) sleep is important for memory

So...after 4 months of being MIA I've finally emerged from the deep, dark, and lonely cave of academia to give a brief update on what I've been doing all this time. When I wasn't furiously working on my dissertation related to working memory and aging, I was making final revisions to a theoretical review paper on sleep and memory. I'm happy to announce that after countless hours of lost sleep (irony?) it's finally been accepted for publication! I'll link the article abstract once it's up. For now let's talk about why NREM sleep is important (and why I needed it so badly for the past few months).

During the early years of sleep research, NREM sleep was discovered to play a role in the restoration of physiological functions (Siegal, 2005). However, relatively recently it's been established to play an equally important function, that of sleep-dependent memory consolidation. Some may be asking, "what the bleep is NREM sleep?" Here's the technical answer according to the American Academy of Sleep Medicine. It consists of 3 stages (N1, N2, and N3, very original...) N1 consists of low amp electrical activity measured by electroencephalogram (EEG) where slow eye movements take place. During N2, you're unconscious, but easily awoken. Here, we find seemingly weird blips in electrical brain activity known as k-complexes and sleep spindles. Sleep spindles are super important for memory consolidation, as will be discussed later. N3 (or slow wave sleep) consists of delta waves and peak to peak amps >75uV found in frontal lobes, also very important for sleep-dependent memory consolidation. Now how does all of this electrical activity consolidate memory?

In the early 1970s Ekstrand and colleagues observed that slow wave sleep was positively correlated with the ability to retain a word pair-associate list, while rapid eye movement (REM) sleep was not. They went on to publish their findings in Science. Memorizing these word pairs depend on declarative memory system functioning. Declarative memory is hippocampal-based memory accessible through conscious recollection including facts and events. Ekstrand's findings and many other subsequent studies firmly established that slow wave sleep was indeed important for declarative memory consolidation (check out Diekelmann and Born, 2010 for a comprehensive review).

Another seminal study by Wilson and McNaugton (1994), also published in Science, observed an increased tendency for particular hippocampal place cells that fired during a spatial behavioral task to also fire during subsequent slow wave sleep in rats. This lay the foundation for discovering that memory traces consolidate from short-term to long-term memories by a process involving reactivation of sharp wave-ripples in the hippocampus during sleep.

In a more recent and very cool study, Born and colleagues (2007) had human subject learn card pair locations while smelling different odors simultaneously (the top left card paired with the scent of my feet, for example). When the researchers reintroduced those same smells during the subjects' slow wave sleep (my feet in the poor subject's face), memory for the card pair locations (top left card) tied to those smells (my feet) were enhanced at recall the next day. Also, through fMRI they saw reactivation of the hippocampus during slow wave sleep. In an alternative study, they used transcranial magnetic stimulation to essentially boost slow oscillations during NREM sleep, which not only increased slow wave sleep and sleep spindles, but also enhanced declarative memory consolidation.

From these findings they developed a model postulating that slow waves originating from the neocortex synced both hippocampal sharp waves and thalamocortical sleep spindles, resulting in primed cortical networks for long-term memory storage. The research team was the first to provide empirical support for a causal role of hippocampal memory reactivation for memory enhancement during sleep.

The key point I'm trying to emphasize here is that slow wave sleep and sleep spindle activity are essential for sleep dependent declarative memory consolidation.

The question I pose in my paper (with the invaluable help of Dr. Robert Göder) is what happens to declarative memory consolidation when slow wave sleep and sleep spindle activity, both taking place during NREM sleep, are disrupted? I've definitely experienced the detrimental effects first hand and hope to soon show you, with the latest research, how abnormal NREM sleep can really mess with memory consolidation. For now, I return to my cave to rest my weary head, praying that I don't become an unfortunate case of ABD (all but dissertation) due to lack of sleep.

References:

Siegel, J. (2005). Clues to the functions of mammalian sleep Nature, 437 (7063), 1264-1271 DOI: 10.1038/nature04285

Iber C, Ancoli-Israel S, Chesson A, Quan SF for the American Academy of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated Events : Rules, Terminology and Technical Specifications, 1st ed. : Wenchester, Minois, American Academy of Sleep Medicine 2007.

Diekelmann, S., & Born, J. (2010). The memory function of sleep Nature Reviews Neuroscience DOI: 10.1038/nrn2762

Fowler MJ, Sullivan MJ, Ekstrand BR. Sleep and memory. Science 1973;79:302-304.

Wilson, M., & McNaughton, B. (1994). Reactivation of hippocampal ensemble memories during sleep Science, 265 (5172), 676-679 DOI: 10.1126/science.8036517

Rasch B, Büchel C, Gais S, & Born J (2007). Odor cues during slow-wave sleep prompt declarative memory consolidation. Science (New York, N.Y.), 315 (5817), 1426-9 PMID: 17347444

Marshall, L., Helgadóttir, H., Mölle, M., & Born, J. (2006). Boosting slow oscillations during sleep potentiates memory Nature, 444 (7119), 610-613 DOI: 10.1038/nature05278