Memory Consolidation and Its Connection to the Quality of Sleep

While is it widely accepted that a great deal of our life spent asleep contributes to our memory formation, the complex phenomena between our biological function and memory consolidation has formed an indefinite relationship due to the myriad stages of sleep and memory types known. As such, this literature will first broadly define the used terms memory consolidation and sleep, followed by a presentation of the converging evidence for sleep-dependent memory consolidation through molecular and behavioural studies. As a result, the previous belief denoting a passive improvement in memory consolidation due to reduced interference from external stimuli, has diverted to the current speculation revealing active consolidation of memory during one's sleep.

In the course of the waking brain, Memory function is initiated through the encoding of sensorimotor experiences acquired via stimuli perception. This labile memory representation then undergoes memory consolidation- a process of stabilising a newly acquired memory trace by remodelling of synapses and spines of neurons in the brain on a Molecular, cellular, and systems-level process. Brain plasticity, a stimuli response forming lasting structural and functional neural changes, allows these consolidated memory traces to be integrated into one's existing knowledge networks for permanent storage. As the memory, or neuronal representation, is susceptible to degradation (E.g. forgetting) through interference of new stimuli, consolidation also involves reactivation of stabilised memories for active retention, forming an optimally integrated memory commonly known as long term memory.

Furthermore, Sleep refers to a state of reduced responsiveness to stimuli during a reversible condition of lost consciousness. Contrasting to earlier findings, mammalian sleep consists of two core stages: Non-rapid eye-movement sleep (N-REM) consisting of the the slow wave sleep phase (SWS), as well as the rapid eye movement sleep (REM). In humans, these stages alternate cyclically through 90-minute intervals. During these periods of reduced stimuli processing, sleep offers an ideal time to consolidate memories. The sleep-dependent memory consolidation theory is tested through compelling body of research human and animal subjects against task performance to reveal its direct relationship.

At the molecular level, significant number of genes appear to be upregulated in brain tissue during sleep. Animal studies using high density microarray revealed an up-regulation of genes, such as kinase IV, responsible for contribution to brain plasticity and memory consolidation. Further, the upregulation of the synaptic plasticity-associated immediate-early gene (IEG) zif-268 during SWS and REM sleep were seen in rats with rich sensorimotor exposure (E.g. direct electrical stimulation of the hippocampus) during the waking period, whereas a down regulation was found in non-exposed controls in both sleep phases. Similarly, in humans, regional brain activation during daytime task training were later found reactivated in their REM sleep. This molecular evidence for sleep-dependent memory consolidation is therefore represented by a window of increased neuronal plasticity during sleep phases following enriched waking experiences, indicating the synaptic consolidation of long-term memory.

In a similar stance, behavioural experimentations in humans and rats have shown consistent results for sleep-dependent memory consolidation. Most study outcomes resulted in. Memory enhancement studies using motor sequence and visual texture discrimination tasks performed by Stickgold consistently exhibited an increase of REM sleep following task training, whilst also revealing the consolidation of information through an improvement in subsequent task performance. Furthermore, brain imaging studies revealed increased activation of primary visual and motor regions in the brain following a night of sleep, suggesting not only the consolidation of learnt tasks, but also the alteration of strategy allowing for an automatic execution. In contrast, SWS and REM sleep deprivation were correlated with decreased performance skills through human and rat trials, even when retesting is delayed until a week after the end of deprivation. From this perspective, the enhancement phase of memory consolidation has shown to cause either the active retention of a memory instead of its decay, or the enhancement of a memory from producing additional learning

Consequently, converging evidence from a range of behavioural and molecular for the sleep-dependent memory consolidation theory not only diverges from the previously believed notion in which sleep was utilised only to reduce external stimuli present, but also brought the enhancement of memory into light.