Effects of Olanzapine on Slow Wave Sleep, Sleep Spindles and Sleep-Related Memory Consolidation in Schizophrenia

Göder, Robert; Fritzer, Gunther; Gottwald, Birgit; Lippmann, B.; Seeck‐Hirschner, Mareen; Serafin, I; Aldenhoff, Josef B.

doi:10.1055/s-2007-1004592

Cited by 75 publications

(55 citation statements)

References 43 publications

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“…Legault et al (721) reported that the dopamine receptor blocker flupenthixol infused into the dorsal striatum 0 -4 h after learning during "REM sleep windows" exerted the same impairing effect on habit consolidation as observed after scopolamine. In humans, so far only patients (with early Parkinson disease and schizophrenia) have been examined in this context with dopaminergic drugs that were partly rather unspecific (465,776). No consistent effects of the treatments on overnight retention of procedural or declarative memories were found in these patients.…”

Section: Neuro-and Hormonal Modulation Associated With Rem Sleep Andmentioning

confidence: 99%

About Sleep's Role in Memory

Rasch

Born

2013

Physiological Reviews

2,265

2,026

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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.

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Section: Neuro-and Hormonal Modulation Associated With Rem Sleep Andmentioning

confidence: 99%

About Sleep's Role in Memory

Rasch

Born

2013

Physiological Reviews

2,265

2,026

View full text Add to dashboard Cite

show abstract

“…SWS duration was positively correlated with memory performance in patients but not in controls (the lack of correlation in controls may have been due to a ceiling effect on performance). A subsequent study found that greater SWS duration was associated with better verbal declarative memory the following morning in chronically medicated schizophrenia patients (Göder et al 2008). Furthermore, enhancing slow waves using transcranial direct current stimulation during NREM sleep improved verbal memory retention in medicated schizophrenia patients (Göder et al 2013).…”

Section: Sleep-specific Eeg Rhythms In Schizophreniamentioning

confidence: 98%

Sleep and Plasticity in Schizophrenia

Sprecher

Ferrarelli²,

Benca³

2015

Sleep, Neuronal Plasticity and Brain Function

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Schizophrenia is a devastating mental illness with a worldwide prevalence of approximately 1 %. Although the clinical features of the disorder were described over one hundred years ago, its neurobiology is still largely elusive despite several decades of research. Schizophrenia is associated with marked sleep disturbances and memory impairment. Above and beyond altered sleep architecture, sleep rhythms including slow waves and spindles are disrupted in schizophrenia. In the healthy brain, these rhythms reflect and participate in plastic processes during sleep. This chapter discusses evidence that schizophrenia patients exhibit dysfunction of sleep-mediated plasticity on a behavioral, cellular, and molecular level and offers suggestions on how the study of sleeping brain activity can shed light on the pathophysiological mechanisms of the disorder.

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“…This contrast with reports of disrupted sleep in SZ (reviewed above) may reflect that sleep disruption primarily characterizes more acute phases of SZ and that APDs are sedating and tend to normalize sleep architecture (18). The effects of chronic APD treatment on spindles are unknown but a single dose of olanzapine in SZ reduced spindle density (78), and acute administration of haloperidol to healthy participants did not affect spindle density (79). …”

Section: Sleep Spindle Deficit In Szmentioning

confidence: 99%

Reduced Sleep Spindles in Schizophrenia: A Treatable Endophenotype That Links Risk Genes to Impaired Cognition?

Manoach

Pan

Purcell

et al. 2016

Biological Psychiatry

190

155

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Although schizophrenia is defined by waking phenomena, abnormal sleep is a common feature. In particular, there is accumulating evidence of a sleep spindle deficit. Sleep spindles, a defining thalamocortical oscillation of non-rapid eye movement Stage 2 sleep, correlate with IQ and are thought to promote long-term potentiation and enhance memory consolidation. Here we review evidence that reduced spindle activity in schizophrenia is an endophenotype that impairs sleep-dependent memory consolidation, contributes to symptoms and is a novel treatment biomarker. Studies showing that spindles can be pharmacologically enhanced in schizophrenia and that increasing spindles improves memory in healthy individuals suggest that treating spindle deficits in schizophrenia may improve cognition. Spindle activity is highly heritable and recent large-scale genome-wide association studies have identified schizophrenia risk genes that may contribute to spindle deficits and illuminate their mechanisms. For example, the schizophrenia risk gene CACNA1I encodes a calcium channel that is abundantly expressed in the thalamic spindle generator and plays a critical role in spindle activity in a mouse knockout. Future genetic studies of animals and humans can delineate the role of this and other genes in spindles. Such cross-disciplinary research, by forging empirical links in causal chains from risk genes to proteins and cellular functions, through to endophenotypes, cognitive impairments, symptoms and diagnosis, has the potential to advance the mechanistic understanding, treatment and prevention of schizophrenia. This review highlights the importance of deficient sleep-dependent memory consolidation among the cognitive deficits of schizophrenia and implicates reduced sleep spindles as a potentially treatable mechanism.

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Effects of Olanzapine on Slow Wave Sleep, Sleep Spindles and Sleep-Related Memory Consolidation in Schizophrenia

Abstract: Since not only slow wave sleep but also sleep spindles are supposed to promote sleep-related memory consolidation, we suggest that a putative positive effect on memory performance by slow wave sleep augmentation is neutralised by the decrease in sleep spindles due to olanzapine.

Cited by 75 publications

References 43 publications

About Sleep's Role in Memory

About Sleep's Role in Memory

Sleep and Plasticity in Schizophrenia

Reduced Sleep Spindles in Schizophrenia: A Treatable Endophenotype That Links Risk Genes to Impaired Cognition?

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