Sleep and memory
Memory, the cognitive process of storing and retrieving past experiences, learning and recognition,[1] is a product of brain plasticity, the structural changes within synapses that create associations between stimuli.
In 1801, David Hartley first suggested that dreaming altered the associative planetary links within the brain during rapid eye movement (REM) periods of the sleep cycle.
Barrie wrote ‘It is the nightly custom of every good mother after her children are asleep to rummage in their minds and put things straight for next morning, repacking into their proper places the many articles that have wandered during the day....When you wake in the morning, the naughtinesses and evil passions with which you went to bed have been folded up small and placed at the bottom of your mind; and on the top, beautifully aired, are spread out your prettier thoughts, ready for you to put on.’ The stories of Peter Pan take place in a fictional world and contain many allusions to aspects of cognitive psychology, some of which predate their formal scientific investigation.
Wakefulness is found through an electroencephalogram (EEG) which is measured and characterized by beta waves, the highest in frequency but lowest in amplitude, and tend to move inconsistently due to the vast amount of stimuli a person encounters while awake.
[23] A blood-oxygen-level dependent (BOLD) fMRI was used in a study by Drummond et al. to measure the brain's response to verbal learning following sleep deprivation.
The implication of these findings are that the brain can initially compensate for the effects of sleep deprivation while maintaining partially intact performance, which declines with an increasing time-on-task.
This initial compensation may be found in the bilateral regions of both frontal and parietal lobes and the activation of the prefrontal cortex is significantly correlated with sleepiness.
The implication of this finding is that additional brain regions activated after both verbal learning and divided attention tasks following TSD represent a cerebral compensatory response to lacking sleep.
Interfering with SPW-Rs or their coupling with neocortical slow oscillations results in memory impairment, which can be as severe as surgically damaging the hippocampus and/or associated structures.
Researchers used rats in order to investigate the effects of novel tactile objects on the long-term evolution of the major rodent forebrain loops essential in species-specific behaviours, including such structures as the hippocampus, putamen, neocortex and the thalamus.
This study was done to prove that the same hippocampal areas are activated in humans during route learning in a virtual town, and are reactivated during subsequent slow wave sleep (SWS).
These findings prove that learning-dependent modulation in hippocampal activity while sleeping shows processing of the previously learned episodic and spatial memory traces.
[10] Based on the active system consolidation hypothesis, repeated reactivations of newly encoded information in hippocampus during slow oscillations in NREM sleep mediate the stabilization and gradual integration of declarative memory with pre-existing knowledge networks on the cortical level.
Physostigmine is an acetylcholinesterase inhibitor; it is a drug that inhibits the breakdown of the inhibitory neurotransmitter acetylcholine, thereby allowing it to remain active longer in the synapses.
Results showed that the increased ACh negatively affected recall memory (declarative task), in the sleep condition compared to participants given the placebo.
In a study by Fischer and Born, 2009,[36] previous knowledge of monetary reward and post-training sleep are proven to be significant predictors of overall finger sequence tapping performance.
This stage of sleep is characterized by muscle atonia, fast but low voltage EEG and, as the name suggests, rapid eye movement.
In a Hennevin et al. study, 1989,[38] the mesencephalic reticular formation (MRF) was given light electrical stimulation, during REM sleep, which is known to have an advantageous effect for learning when applied after training.
There is no guarantee as to what functions REM sleep may perform for our bodies and brains, but modern research is always expanding and assimilating new ideas to further our understanding of such processes.
Peigneux et al., 2006,[40] reported that the lateral geniculate nucleus and occipital cortex display higher levels of activity during REM sleep than during wakefulness.
[37][41] In a study using post learning REM sleep deprivation the effects of stimulating the P wave generator (located in the pontine tegmentum) of a rat were observed.
It is hypothesized that brain mechanisms during REM sleep, as well as pure repetition priming, can account for the implicit recognition of the previously shown faces.
[43] However, control subjects did not complete a SRT task, thus researchers could not assume the reactivation of certain networks to be a result of the implicitly learned sequence/grammar as it could simply be due to elementary visuomotor processing which was obtained in both groups.
Results showed that the rats in the REM sleep deprivation group experienced decreased levels of brain-derived neurotrophic factor in the cerebellum (coordination, motor learning) and brainstem (sensory and motor ascending pathway); conversely, the hippocampus (long-term memory, spatial navigation), showed decreases in nerve growth factor levels.
FMRI output for the night-sleep group indicated increased activation in the right primary motor cortex/M1/Prefrontal Gyrus (contra lateral to the hand they were block tapping with), right anterior medial prefrontal lobe, right hippocampus (long-term memory, spatial memory), right ventral striatum (olfactory tubercle, nucleus accumbens), as well as regions of the cerebellum (lobules V1, V11).
[1] Considered to be a mental workspace enabling temporary storage and retrieval of information, working memory is crucial to problem-solving and analysis of different situations.
Sleep deprivation was found to interrupt the slow processes that lead to learning of this procedural skill and alter connectivity changes that would have normally been seen after a night of rest.
Neuroplasticity has been thoroughly researched over the past few decades and results have shown that significant changes that occur in our cortical processing areas have the power to modulate neuronal firing to both new and previously experienced stimuli.
In a different study it was found that there was a sleep related increase in calmodulin-dependent protein kinase IV that has been specifically involved in synaptic depression and in the consolidation of long-term memory.
[60] To combat this, donepezil has been tested in healthy elderly patients where it was shown to increase time spent in REM sleep and improve following day memory recall.
