Sleep memory processing: the sequential hypothesis

Abstract

According to the sequential hypothesis (SH) memories acquired during wakefulness are processed during sleep in two serial steps respectively occurring during slow wave sleep (SWS) and rapid eye movement (REM) sleep. During SWS memories to be retained are distinguished from irrelevant or competing traces that undergo downgrading or elimination. Processed memories are stored again during REM sleep which integrates them with preexisting memories. The hypothesis received support from a wealth of EEG, behavioral, and biochemical analyses of trained rats. Further evidence was provided by independent studies of human subjects. SH basic premises, data, and interpretations have been compared with corresponding viewpoints of the synaptic homeostatic hypothesis (SHY). Their similarities and differences are presented and discussed within the framework of sleep processing operations. SHY’s emphasis on synaptic renormalization during SWS is acknowledged to underline a key sleep effect, but this cannot marginalize sleep’s main role in selecting memories to be retained from downgrading traces, and in their integration with preexisting memories. In addition, SHY’s synaptic renormalization raises an unsolved dilemma that clashes with the accepted memory storage mechanism exclusively based on modifications of synaptic strength. This difficulty may be bypassed by the assumption that SWS-processed memories are stored again by REM sleep in brain subnuclear quantum particles. Storing of memories in quantum particles may also occur in other vigilance states. Hints are provided on ways to subject the quantum hypothesis to experimental tests.

Targeted memory reactivation of newly learned words during sleep triggers REM-mediated integration of new memories and existing knowledge

“…Such findings are in line with several theories proposing that SWS and REM play complementary roles (Giuditta, 2014;Diekelmann & Born, 2010;Ribeiro et al, 2007;Ficca et al, 2004;Stickgold et al, 2000). These theories broadly share the view that SWS strengthens recent memories through spontaneous reactivation, and selecting memories to be retained or forgotten.…”

Effect of castration on the susceptibility of male rats to the sleep deprivation-induced impairment of behavioral and synaptic plasticity

“…Rather, it replicates the assumptions that SD-induced memory impairment is primarily attributed to an alteration of vigilance state quantities. Accordingly, the sequential hypothesis (SH) claims that SD-induced memory deficits are based on altered proportion of different phases of sleep (Giuditta, 2014;Ota, Moreira, et al, 2013). In addition to these well-known effects on cognitive functions, several neurotransmitters, cellular and molecular factors involved in synaptic plasticity within the hippocampus of rodents have also been shown to be influenced by SD (Guzman-Marin et al, 2006;Longordo, Kopp, et al, 2009;Ravassard et al, 2009).…”

Ovariectomy does not exacerbate the negative effects of sleep deprivation on synaptic plasticity in rats

“…Rather, it reflects the assumptions that SD-induced memory impairment is mainly attributed to an alteration of vigilance state quantities. According to the sequential hypothesis (SH), SD-induced memory deficits are based on changes in proportion among the different phases of sleep [53,54]. Parallel to these well-documented effects on cognitive functions, several neurotransmitters, cellular and molecular correlates of synaptic plasticity within the hippocampus of experimental animals have also been shown to be influenced by SD [15][16][17].…”