#memory consolidation
Scrap the nap: Study shows short naps don’t relieve sleep deprivation
A nap during the day won’t restore a sleepless night, says the latest study from Michigan State University’s Sleep and Learning Lab.
“We are interested in understanding cognitive deficits associated with sleep deprivation. In this study, we wanted to know if a short nap during the deprivation period would mitigate these deficits,” said Kimberly Fenn, associate professor of MSU, study author and director of MSU’s Sleep and Learning Lab. “We found that short naps of 30 or 60 minutes did not show any measurable effects.”
The study was published in the journal Sleep and is among the first to measure the effectiveness of shorter naps — which are often all people have time to fit into their busy schedules.
“While short naps didn’t show measurable effects on relieving the effects of sleep deprivation, we found that the amount of slow-wave sleep that participants obtained during the nap was related to reduced impairments associated with sleep deprivation,” Fenn said.
Slow-wave sleep, or SWS, is the deepest and most restorative stage of sleep. It is marked by high amplitude, low frequency brain waves and is the sleep stage when your body is most relaxed; your muscles are at ease, and your heart rate and respiration are at their slowest.
“SWS is the most important stage of sleep,” Fenn said. “When someone goes without sleep for a period of time, even just during the day, they build up a need for sleep; in particular, they build up a need for SWS. When individuals go to sleep each night, they will soon enter into SWS and spend a substantial amount of time in this stage.”
Fenn’s research team – including MSU colleague Erik Altmann, professor of psychology, and Michelle Stepan, a recent MSU alumna currently working at the University of Pittsburgh - recruited 275 college-aged participants for the study.
The participants completed cognitive tasks when arriving at MSU’s Sleep and Learning Lab in the evening and were then randomly assigned to three groups: The first was sent home to sleep; the second stayed at the lab overnight and had the opportunity to take either a 30 or a 60 minute nap; and the third did not nap at all in the deprivation condition.
The next morning, participants reconvened in the lab to repeat the cognitive tasks, which measured attention and placekeeping, or the ability to complete a series of steps in a specific order without skipping or repeating them — even after being interrupted.
“The group that stayed overnight and took short naps still suffered from the effects of sleep deprivation and made significantly more errors on the tasks than their counterparts who went home and obtained a full night of sleep,” Fenn said. “However, every 10-minute increase in SWS reduced errors after interruptions by about 4%.”
These numbers may seem small but when considering the types of errors that are likely to occur in sleep-deprived operators — like those of surgeons, police officers or truck drivers — a 4% decrease in errors could potentially save lives, Fenn said.
“Individuals who obtained more SWS tended to show reduced errors on both tasks. However, they still showed worse performance than the participants who slept,” she said.
Fenn hopes that the findings underscore the importance of prioritizing sleep and that naps — even if they include SWS — cannot replace a full night of sleep.
For the first time, scientists in the Center for Interdisciplinary Research in Biology (CNRS/INSERM/Collège de France) have produced direct evidence that the long-term storage of memories involves a dialogue between two brain structures, the hippocampus and cortex, during sleep; by enhancing this dialogue, they succeeded in triggering the consolidation of memories that would otherwise have been forgotten. This work was published in Nature Neuroscience on 16 May 2016.
Since the 1950s, the principal theories on memory have posited that such traces are initially formed in the hippocampus and then gradually transferred to the cortex for long-term storage. Although supported by numerous experimental studies, this hypothesis had never yet been directly verified.
In order to prove it, the scientists first recorded the activity of the hippocampus and cortex during sleep. They found a correlation between the oscillations observed in these two structures: when the hippocampus emitted sharp wave-ripples, the cortex in turn emitted delta waves and spindles like a series of questions and answers. To establish a link with memory, the scientists then trained rats to memorize the position of two identical objects in a room. During testing the next day, one of the objects had been moved and the rodents had to determine which one. Those that had spent 20 minutes in the room on the first day passed the test, while those that had only been there for three minutes failed. This difference was also reflected in the hippocampal-cortical coupling during sleep just after the initial exploration: coupling was more visible in rats that passed the test the next day. It was then necessary to prove that this was indeed the cause of memorization.
The scientists then developed a system for real-time detection of hippocampal sharp wave-ripples and immediate triggering of cortical delta waves and spindles, or in other words to generate coupling between these two structures on demand. They applied this system in rats that had been trained for just three minutes the first day, and were therefore not expected to remember the position of the objects the next day: these rodents passed the test perfectly. By contrast, if a variable delay was introduced between the hippocampal and cortical waves, the effect disappeared.
To better understand the mechanisms at play, the scientists also recorded cortical activity during learning, sleep and the test. They observed that selected neurons changed their activity in the context of coupling during sleep, and that the next day the cortex responded to the task by becoming more active in the vicinity of the object that had been moved.
By demonstrating the mechanisms underlying long-term memorization, this work may shed new light on certain memory disorders in humans. It might thus be possible to envisage overcoming certain memory deficits if they result from the same mechanism as that studied here. However, the ethical issues related to these techniques will need to be addressed and methods will have to be refined to enable selective action on the memories that need to be enhanced, before any clinical application can be envisaged. The team is now set to elucidate the dialogue between the hippocampus and cortex, notably when several memories need to be remembered, or not.
We tend to think our memory works like a filing cabinet. We experience an event, generate a memory and then file it away for later use. However, according to medical research, the basic mechanisms behind memory are much more dynamic. In fact, making memories is similar to plugging your laptop into an Ethernet cable—the strength of the network determines how the event is translated within your brain.
Neurons (nerve cells in the brain) communicate through synaptic connections (structures that pass a signal from neuron-to-neuron) that “talk” to each other when certain neurotransmitters (chemicals that allow the transmission of these signals) are present.
Think of a neurotransmitter as an email. If you’re busy and you receive one or two emails, you might ignore them. But, if you are bombarded with hundreds of emails from the same person, saying basically the same thing, all at the same time, you will likely begin to pay attention and start a conversation with the sender: Why on earth are you sending me all these emails?
Similarly, neurons only open a line of communication with each other when they receive stimulation from several of the same neurotransmitters at once: Oh, my neighbor keeps hitting me with the same signal? I better talk to them! So, how exactly does this relate to memory? It’s the strength of these connections between neurons that determines how a memory is formed.
“The persistent strengthening of these activated synapses (connections) between neurons is called long-term potentiation (LTP),” said William Griffith, Ph.D., a cellular neuroscientist and chair of the Department of Neuroscience and Experimental Therapeutics at the Texas A&M Health Science Center College of Medicine. “LTP is the most recognized cellular mechanism to explain memory because it can alter the strength between brain cell connections. If this strength is maintained, a memory can be formed.”
LTP happens when nerve cells “fire” or talk to one another at an elevated rate without further increased stimulation from neurotransmitters. In a sense, it’s like building a relationship with the email sender. Once you’ve started a dialogue with the sender you’re in a better position to communicate more easily and maintain a strong rapport. Just like you might add the sender to your contact list, your brain has created a ‘strengthened synaptic contact.’ But, if you’re not talking, the relationship wanes.
Likewise, your ability to recall and remember certain memories depends on maintaining the strength of this long-term connection between synaptic contacts. LTP acts as an Ethernet cable of sorts—allowing your brain to upload, download and process at a higher rate—which may explain why some memories are more vivid than others: the pathway on which you contact them performs at a faster pace.
“The brain is a plastic organ,” Griffith explained. “This means it can easily reconfigure or modify itself. However, it’s also a muscle. You use it or you lose it. As the synapses and pathways between neurons are used, they gain the ability to become strengthened or permanently enhanced. This is the building block of how memory works.”
In the same vein, losing this strong LTP— or heightened synaptic connections between neurons—could be the reason behind cognitive loss and impairment. “Because the brain is an organ, it will show wear and tear,” Griffith continued. “Many people believe this decrease in neurons ‘talking’ to one another is responsible for cognitive loss—because the pathways are not being used or strengthened. Just as muscles in the body atrophy when you don’t use them, the brain will deteriorate when it’s not stimulated.”
Griffith said the argument about how memory is consolidated and retrieved is vast, and there are many aspects that still need to be studied about the phenomenon. “When you look at or smell something, it contributes to your memory of an event,” he said. “This can be mapped in many parts of the brain. Memory may also be involved in certain behaviors like addiction. Why does this happen? Is it because the pathways for addiction are strengthened, or because they’re repressed? We don’t know yet.”
The science behind memory is a complex one, and will likely be studied for decades to come. “Many different pathways in the brain interact to set up complex circuits for different types of memories,” Griffith said. “There’s much debate and more research that needs to be done to fully comprehend how our brain generates, consolidates and retrieves memories.”
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