Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

https://www.zora.uzh.ch/id/eprint/77770/1/physiol_rev_93.pdf

About sleep's role in memory

/pdf/exogenous-and-endogenous-components-in-circadian-rhythms-kkmlkwvyoq.pdf

Exogenous and endogenous components in circadian rhythms.

The hyperp las t ic alveolar nodules, which norma l ly occur in the m a m m a r y glands of mice f rom susceptible s t ra ins infected wi th the m a m m a r y tumor virus, are general ly thought to be precancerous. This belief is suppor ted by considerable indirect evidence. Ear l ie r work on hyperp las t ic nodules in mouse m a m m a r y tumorigenesis has been reviewed extensively (2, 4-8, 10). The assumed precancerous na tu re of hyperplast ic alveolar nodules implies t h a t m a m m a r y tumors arise more f requent ly f rom nodules t h a n f rom normal m a m m a r y tissue. Di rec t evidence can be obta ined if exper imenta l condi t ions outl ined by F a u l k i n and D e O m e (4) can be met . This report presents three series of exper iments which fulfill the essential exper imenta l condit ions and which provide the desired direct evidence. I n addit ion, a new t r ansp lan ta t ion technic is described, which permi t s the t r ansp lan ta t ion of normal , nodular , and tumorous m a m m a r y tissues into host m a m m a r y fa t pads freed f rom host m a m m a r y tissue, and the subsequent deve lopment of character is t ic pa t te rns of outgrowth. I n each of the three exper imenta l series, nodules and samples of normal m a m m a r y tissue were transp lan ted into sites freed from host m a m m a r y tissue, and the n u m b e r of tumors derived f rom these t ransp lan ts was determined. Tissue samples were t r ansp lan ted e i ther into the dorsal subcutis , into gland-free (cleared) inguinal (#4) m a m m a r y fa t pads, or first into the subcutaneous sites and then re t ransp lan ted into the fa t pads. T h e three series of exper iments are presented under the following headings: (a) \"Longt e rm t r ansp lan ta t ion into the dorsal subcu t i s\" ; (b) \"Longte rm t r ansp lan ta t ion into cleared m a m m a r y fa t p a d s \" ; and (c) \"Ret r ansp lan ta t ion of long-term subcutaneous transp lan ts into cleared m a m m a r y fa t pads . \

Development of mammary tumors from hyperplastic alveolar nodules transplanted into gland-free mammary fat pads of female C3H mice.

Brain serotonin cocentrations at 1 p.m. were significantly elevated 1 hour after rats received a dose of L-tryptophan (12.5 milligrams per kilogram. intraperitoneally) smaller than one-twentieth of the normal daily dietary intake. Plasma and brain tryptophan levels were elevated 10 to 60 minutes after the injection, but they never exceeded the concentrationis that occur nocturnally in untreated aninmals as result of their normal 24-hour rhythms. These data suggest that physiological changes in plasma tryptophan concentration influenice brain serotonin levels.

https://science.sciencemag.org/content/sci/173/3992/149.full.pdf

Brain serotonin content: physiological dependence on plasma tryptophan levels.

Eosinophils are specialized myeloid cells associated with allergy and helminth infections. Blood eosinophils demonstrate circadian cycling, as described over 80 years ago, and are abundant in the healthy gastrointestinal tract. Although a cytokine, interleukin (IL)-5, and chemokines such as eotaxins mediate eosinophil development and survival, and tissue recruitment, respectively, the processes underlying the basal regulation of these signals remain unknown. Here we show that serum IL-5 levels are maintained by long-lived type 2 innate lymphoid cells (ILC2) resident in peripheral tissues. ILC2 cells secrete IL-5 constitutively and are induced to co-express IL-13 during type 2 inflammation, resulting in localized eotaxin production and eosinophil accumulation. In the small intestine where eosinophils and eotaxin are constitutive, ILC2 cells co-express IL-5 and IL-13; this co-expression is enhanced after caloric intake. The circadian synchronizer vasoactive intestinal peptide also stimulates ILC2 cells through the VPAC2 receptor to release IL-5, linking eosinophil levels with metabolic cycling. Tissue ILC2 cells regulate basal eosinophilopoiesis and tissue eosinophil accumulation through constitutive and stimulated cytokine expression, and this dissociated regulation can be tuned by nutrient intake and central circadian rhythms.

/pdf/type-2-innate-lymphoid-cells-control-eosinophil-homeostasis-4rfh9jq7af.pdf

Type 2 innate lymphoid cells control eosinophil homeostasis

SummaryLight-synchronized periodicity analysis reveals a susceptibility rhythm in C mice to E. coli endotoxin. Susceptibility varies predictably and significantly along the 24-hour time scale. A dose of endotoxin which is compatible with survival of most animals when given during middle of daily dark period is highly lethal when it is given 8-12 hours earlier or later. LD50 also was determined for 2 samples from identical batch of endotoxin tested 12 h apart on separate groups of comparable C mice kept under conditions standardized for periodicity analysis: Differences in potency significant at 1% were seen at 2 dose levels common to both assays, the computed “potency ratio” being 3.22.

Susceptibility rhythm to E. coli endotoxin and bioassay.

Eosinophil rhythm in mice: range of occurrence; effects of illumination, feeding, and adrenalectomy.

SummaryDaily rhythms were studied in I mice of several age groups under standardized experimental circumstances. The rhythms in eosinophil count and in rectal temperature are described for this stock. Moreover, 24-hour periodicities are noted for the susceptibility of I mice to audiogenic convulsions and for their ability to recover from convulsions. The magnitude of these differences was large and was statistically significant. In one group of young animals the convulsive risk was 11% by day and 63% by night and in another, 0% by day and 85% by night. Changes with age in several of the variables studied are also noted.

24-Hour periodicity and audiogenic convulsions in I mice of various ages.

Any advances in our knowledge about the genesis of mammary cancer in mice may be attributed primarily to the availability of homozygous or inbred stocks. For research these strains are to the biologist as pure chemicals are to the chemist. If this analogy may be justified, one striking distinction should be mentioned, however. Whereas chemicals are generally stable over a long period of time, mice, like all living forms, are subject to \"mutational\" changes which may occur at any time regardless of the degree of inbreeding. Just as many investigators are interested in the biological effects of mutations induced by carcinogenic agents, investigators trained in genetics are constantly on the alert for mutations that occur spontaneously in control strains. If these are recognized they might compare with the synthesis of new chemicals, new \"tools\" for research; if they go unnoticed, the experimental results may be distorted because of the changes in the genetic constitution of the experimental animals and, therefore, may become the basis for new theories which cannot be confirmed. One purpose of this report is to review the resuits that have been secured by various investigators on the development of mammary cancer in mice, another is to bring together in a single article the observations from many analogous experiments which are now scattered throughout the literature. Some additional material will be included.

/pdf/some-enigmas-associated-with-the-genesis-of-mammary-cancer-4hvyb3els4.pdf

Some enigmas associated with the genesis of mammary cancer in mice.

https://science.sciencemag.org/content/sci/128/3325/657.full.pdf

Audiogenic abnormality spectra, twenty-four hour periodicity, and lighting.

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