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Sleep & Memory/Review
Sleep, dreams, and memory consolidation: The role of the stress hormone cortisol

Jessica D. Payne and Lynn Nadel¹

The University of Arizona, Department of Psychology, Tucson, Arizona 85721, USA

ABSTRACT

We discuss the relationship between sleep, dreams, and memory, proposing that the content of dreams reflects aspects of memory consolidation taking place during the different stages of sleep. Although we acknowledge the likely involvement of various neuromodulators in these phenomena, we focus on the hormone cortisol, which is known to exert influence on many of the brain systems involved in memory. The concentration of cortisol escalates over the course of the night's sleep, in ways that we propose can help explain the changing nature of dreams across the sleep cycle.

Article and publication are at http://www.learnmem.org/cgi/doi/10.1101/lm.77104.

² This observation seems, at first glance, to conflict with the fact that CA3 is highly susceptible to the toxic effects of chronic stress (Sapolsky, 2000). However, the impact of acute and chronic stress clearly differs in a number of ways, and this conflict may be more apparent than real.

³ Not all glucocorticoid effects on memory are negative. For example, there is ample evidence that glucocorticoids released during or after emotionally arousing experiences play a critical role in the formation of lasting memories (Roozendaal 2003), and memory for emotional materials is actually facilitated by cortisol (see Buchanan and Lovallo 2001; J.D. Payne, E.D. Jackson, S. Hoscheidt, W.J. Jacob, and L. Nadel, in prep.). Memory for emotionally neutral experiences, by contrast, is typically negatively affected by acute stressors or administration of cortisol (for a review, see Payne et al. 2004). Along these lines it is interesting to note that many dreams are distinctly emotional, often involving intense fear, and that emotional dreams are among the most well-remembered.

⁴ Although Gais and Born (2004) failed to show a corresponding increase in cortisol after administration of a small dose of the acetylcholine agonist physostigmine (0.75 mg), it remains possible that higher levels of acetylcholine may trigger a concomitant rise in cortisol.

Corresponding author.

¹ E-mail nadel{at}u.arizona.edu; fax (520) 621-9306.

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