title: Sleep-induced changes in associative memory.
abstract: The notion that dreaming might alter the strength of associative links in memory was first proposed almost 200 years ago. But no strong evidence of such altered associative links has been obtained. Semantic priming can be used to quantify the strength of associative links between pairs of words; it is thought to measure the automatic spread of activation from a "node" representing one word to nodes representing semantically related words. Semantic priming could thus be used to test for global alterations in the strengths of associative links across the wake-sleep cycle. Awakenings from REM and nonREM (NREM) sleep produce a period of state carry-over during which performance is altered as a result of the brain's slow transition to full wakefulness, and cognitive testing in this period can provide information about the functioning of the brain during the prior sleep period. When subjects were tested across the night--before and after a night's sleep as well as immediately following forced awakenings from REM and NREM sleep--weak priming (e. g., thief-wrong) was found to be state dependent (p = 0.016), whereas strong priming (e.g., hot-cold) was not (p = 0.89). Weak primes were most effective in the presleep and REM sleep conditions and least effective in NREM and postsleep conditions. Most striking are analyses comparing weak and strong priming within each wake-sleep state. Contrary to the normal pattern of priming, subjects awakened from REM sleep showed greater priming by weak primes than by strong primes (p = 0.01). This result was seen in each of three protocols. In contrast, strong priming exceeded weak priming in NREM sleep. The shift in weak priming seen after REM sleep awakenings suggests that cognition during REM sleep is qualitatively different from that of waking and NREM sleep and may reflect a shift in associative memory systems, a shift that we hypothesize underlies the bizarre and hyperassociative character of REM-sleep dreaming. Known changes in brainstem activity that control the transition into and maintenance of REM sleep provide a possible explanation of this shift.
authors: Massachusetts Medical Health Center, Harvard Medical School, 74 Fenwood Road, Boston, MA 02115, USA. rstickgold@hms.harvard.edu
authors: R
authors: R
authors: Stickgold
authors: L
authors: L
authors: Scott
authors: C
authors: C
authors: Rittenhouse
authors: J A
authors: JA
authors: Hobson
mesh_terms: D000328:Adult; D001245:Association Learning / Q000502:physiology*; D001931:Brain Mapping; D002940:Circadian Rhythm; D004292:Dominance, Cerebral / Q000502:physiology; D004325:Dreams / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D009483:Neuropsychological Tests; D017286:Polysomnography; D011930:Reaction Time; D012660:Semantics; D012890:Sleep / Q000502:physiology*; D012894:Sleep Stages / Q000502:physiology; D012895:Sleep, REM / Q000502:physiology; D014851:Wakefulness / Q000502:physiology