Information

How are our senses dimmed during sleep?


Our senses are not as sensitive during sleep compared to wake. There is an arousal threshold during sleep that only when it is overcome will it wake a person up. My question is how is this arousal threshold lowered as sleep progresses? And how it is raised again during the latter stages of sleep?


At night several changes occur in the body due to absence of sunlight and other surrounding changes. The biological clock inside the body performs certain function in a healthy body whenever changes are sensed.

There are many receptors in our body located on cell membrane. They are made up of proteins and their function is to receive information from neurotransmitters. This information will be sent to specific part of the brain. If we take sensory information then it is Parietal lobe. This lobe receives the sensory information from all over the body and responds to it when body is active. During sleep, the senses that go through the thalamus, are shut down by gating either in the Nucleus Reticularis Thalami (NRT) or in the Thalamus itself. GABAergic inhibition of the thalamus, most likely deriving from the NRT is probably a part of the reason that sensory stimuli doesn't penetrate during sleep.

This is also influenced by release of hormones in the body whose level when rises in the blood causes certain changes in the concentration at some regions such as receptors which gets blocked temporarily and stops signaling the brain. There is a study on how muscle relaxes when we sleep can be found here Muscle sleep. So it is all the neurotransmitters job at the receptors which stops signals going into brain but internal to the brain it will be active controlling other routine works which it has to do when we are asleep.

The main thing to note here is the 5 different stages of sleep such as non-REM and REM sleep. During those stages several changes take place in the body. The below website gives an excellent insight into different changes happening inside the body when body takes rest at night.

Please refer to "What happens to your body while you are asleep".


When you're awake; the sensations around you as well as your mental will, keep your mind active. How the air smells and what needs to be done all contribute to your day. In order to sleep your brain must weaken these receptors significantly, though not enough that if we heard something too loud or unfamiliar (such as a predator), we overlap those boundaries that keep us resting and wake. Now of course i am talking about the middle of the night. As morning arrives the amount of stimuli needed to overcome the wall that is sleep is diminished, allowing something such as the crowing of a rooster to wake us up.


Another lead are sleep spindles, closely related to the RTN as mentioned before. Basically the thalamus enters a state of high-frequency firing to a low-frequency synchronous one, thereby taking the cortex with it. Sleep spindles are slow-wave potentials as apparent on the EEG that block out the normal flow of peripheral sensory information from thalamus to cortex. Basically this leads to a loss of consciousness as one is unaware of its environment. A similar thing occurs during absence epileptic seizures, where patients temporarily loose consciousness as marked by paroxysmal slow-wave EEG activity interrupting the high-frequency EEG associated with consciousness Kostopaulus (2000). Hope this helps.


Blue light may not be as disruptive to our sleep patterns as originally thought

Contrary to common belief, blue light may not be as disruptive to our sleep patterns as originally thought -- according to University of Manchester scientists.

According to the team, using dim, cooler, lights in the evening and bright warmer lights in the day may be more beneficial to our health.

Twilight is both dimmer and bluer than daylight, they say, and the body clock uses both of those features to determine the appropriate times to be asleep and awake.

Current technologies designed to limit our evening exposure to blue light, for example by changing the screen colour on mobile devices, may therefore send us mixed messages, they argue.

This is because the small changes in brightness they produce are accompanied by colours that more resemble day.

The research, which was carried out on mice, used specially designed lighting that allowed the team to adjust colour without changing brightness.

That showed blue colours produced weaker effects on the mouse body clock than equally bright yellow colours.

The findings, say the team, have important implications for the design of lighting and visual displays intended to ensure healthy patterns of sleep and alertness.

The study is published in Current Biology and funded by the Biotechnology and Biological Sciences Research Council.

The body clock uses a specialised light sensitive protein in the eye to measure brightness, called melanopsin, which is better at detecting shorter wavelength photons.

This is why, say the team, researchers originally suggested blue light might have a stronger effect.

However, our perception of colour comes from the retinal cone cells and the new research shows that the blue colour signals they supply reduce the impact on light on the clock.

Dr Tim Brown, from The University of Manchester, said: "We show the common view that blue light has the strongest effect on the clock is misguided in fact, the blue colours that are associated with twilight have a weaker effect than white or yellow light of equivalent brightness.

"There is lots of interest in altering the impact of light on the clock by adjusting the brightness signals detected by melanopsin but current approaches usually do this by changing the ratio of short and long wavelength light this provides a small difference in brightness at the expense of perceptible changes in colour."

He added: "We argue that this is not the best approach, since the changes in colour may oppose any benefits obtained from reducing the brightness signals detected by melanopsin.

"Our findings suggest that using dim, cooler, lights in the evening and bright warmer lights in the day may be more beneficial.

"Research has already provided evidence that aligning our body clocks with our social and work schedules can be good for our health. Using colour appropriately could be a way to help us better achieve that."


The transition to gas and then electric lighting also made shift work easier: no longer did factory workers have to toil under weak candlelight. Working at night means being awake, active and eating during the biological night – and then trying to sleep when the body is in day-mode. People who work night shifts are estimated to lose between one and four hours of sleep per day, which has short-term effects on emotional stability, memory, reasoning, reaction speeds and hand–eye coordination. Chronic sleep deprivation also precedes the onset of Alzheimer’s disease, cancer and various psychiatric illnesses, and is also associated with heart disease, obesity and diabetes. Similar links have been made to disrupted circadian rhythms, another consequence of shift work. If you are eating and active during the biological night, the circadian clocks in your various organs and tissues become desynchronised, meaning they no longer work as efficiently.

British Summer Time was introduced in 1916. The hope was that the extended evening light would encourage participation in outdoor recreation, facilitate military training and reduce industrial energy consumption. There is a significant downside, however: by moving the clocks forwards each spring, and backwards each autumn, we force a change in the timing of our body clocks. In the US, which also seasonally adjusts its time-keeping, a study of high school students – a population that’s already sleep-deprived – suggested their sleep was curtailed by 32 minutes per night in the week following the spring clock change their reaction speeds and vigilance also temporarily reduced. In adults, the transition to summer time has been associated with a 6% increase in “cyberloafing” – spending one’s work time on non-work-related websites – on the Monday after the clock change. From a health perspective, the clock changes are tied to an increased risk of heart attacks, strokes, suicide attempts and psychiatric admissions.


5 Amazing Things Your Brain Does While You Sleep

We spend a third of our lives sleeping, an activity as crucial to our health and well-being as eating. But exactly why we need sleep hasn't always been clear. We know that sleep makes us feel more energized and improves our mood, but what's really happening in the brain and body when we're at rest?

Research has identified a number of reasons that sleep is critical to our health. When we're sleeping, the brain is anything but inactive. In fact, during sleep, neurons in the brain fire nearly as much as they do during waking hours -- so it should come as no surprise that what happens during our resting hours is extremely important to a number brain and cognitive functions.

Here are five incredible things your brain does while you're asleep -- and good reason to get some shuteye tonight:

Makes decisions.

The brain can process information and prepare for actions during sleep, effectively making decisions while unconscious, new research has found.

A recent study published in the journal Current Biology found that the brain processes complex stimuli during sleep, and uses this information to make decisions while awake. The researchers asked participants to categorize spoken words that were separated into different categories -- words referring to animals or objects and real words vs. fake words -- and asked to indicate the category of the word they heard by pressing right or left buttons. When the task become automatic, the subjects were asked to continue but also told that they could fall asleep (they were lying in a dark room). When the subjects were asleep, the researchers began introducing new words from the same categories. Brain monitoring devices showed that even when the subjects were sleeping, their brains continued to prepare the motor function to create right and left responses based on the meaning of the words they heard.

When the participants woke up, however, they had no recollection of the words they heard.

"Not only did they process complex information while being completely asleep, but they did it unconsciously," researchers Thomas Andrillon and Sid Kouider write in the Washington Post. "Our work sheds new light about the brain’s ability to process information while asleep but also while being unconscious."

Creates and consolidates memories.

While you're asleep, the brain is busy forming new memories, consolidating older ones, and linking more recent with earlier memories, during both REM and non-REM sleep. Lack of rest could have a significant affect the hippocampus, an area of the brain involved in memory creation and consolidation.

For this reason, sleep plays a very important role in learning -- it helps us to cement the new information we're taking in for better later recall.

“We’ve learned that sleep before learning helps prepare your brain for initial formation of memories,” Dr. Matthew Walker, a University of California, Berkeley sleep researcher, tells the National Institutes of Health. “And then, sleep after learning is essential to help save and cement that new information into the architecture of the brain, meaning that you’re less likely to forget it.”

Think twice before pulling an all-nighter to study for your next exam: If you don't sleep, your ability to learn new information could drop by up to 40 percent, Walker estimates.

Makes creative connections.

Sleep can be a powerful creativity-booster, as the mind in an unconscious resting state can make surprising new connections that it perhaps wouldn't have made in a waking state.

A 2007 University of California at Berkeley study found that sleep can foster "remote associates," or unusual connections, in the brain -- which could lead to a major "a-ha" moment upon waking. Upon waking from sleep, people are 33 percent more likely to make connections between seemingly distantly related ideas.

Clears out toxins.

A series of 2013 studies found that an important function of sleep may be to give the brain a chance to do a little housekeeping.

Researchers at the University of Rochester found that during sleep, the brains of mice clear out damaging molecules associated with neurodegeneration. The space between brain cells actually increased while the mice were unconscious, allowing the brain to flush out the toxic molecules that built up during waking hours.

If we're not getting enough sleep, our brains don't have adequate time to clear out toxins, which could potentially have the effect of accelerating neurodegenerative diseases like Parkinson's and Alzheimer's.

Learns and remembers how to perform physical tasks.

The brain stores information into long-term memory through something known as sleep spindles, short bursts of brain waves at strong frequencies that occur during REM sleep.

This process can be particularly helpful for storing information related to motor tasks, like driving, swinging a tennis racquet or practicing a new dance move, so that these tasks become automatic. What happens during REM sleep is that the brain transfers short-term memories stored in the motor cortex to the temporal lobe, where they become long-term memories.

"Practice during sleep is essential for later performance," James B. Maas, a sleep scientist at Cornell University, told the American Psychological Association. "If you want to improve your golf game, sleep longer."


Part 2: Understanding our Sleep Behaviors

00:00:07.18 Hello.
00:00:08.18 I'm Ying-Hui Fu from the Department of Neurology at University of California, San Francisco.
00:00:17.20 Today, I'm going to tell you two examples of the mutations that we have found for humans
00:00:25.03 who have advanced sleep phase syndrome.
00:00:29.18 I will also show you how, by studying these mutations, we can actually learn a great deal
00:00:35.15 about the molecular mechanisms of human sleep behavioral regulation.
00:00:41.02 Before I start, I want to first briefly remind you of the core molecular clock.
00:00:47.15 For the mammalian system, there are two major transcription factors, CLOCK and BMAL.
00:00:53.01 They form dimers and bind to the promoter of clock control genes.
00:00:57.22 And PERs and CRYs are the most well studied clock control genes.
00:01:03.11 The protein levels of PERs and CRYs are tightly regulated.
00:01:08.00 And the PER is regulated by casein kinase 1 delta.
00:01:13.14 Another important kinase for circadian regulation is the GSK3 beta.
00:01:19.02 PERs and CRYs can form dimers and then come back to suppress the transcriptional activation
00:01:25.07 of CLOCK and BMAL, therefore forming a feedback. transcriptional feedback loop.
00:01:33.24 The first example I want to tell you is a mutation we found for this family that Louis
00:01:40.16 told you in the first part of this talk.
00:01:44.12 The mutation carriers in this family, they all showed about four hours phase advance.
00:01:50.09 The mutation was found in the gene encoding for casein kinase 1 delta.
00:01:55.24 And the mutation changed the amino acid at 44 from a threonine to alanine.
00:02:03.03 And this mutation makes. the casein kinase 1 has a reduced enzyme activity.
00:02:08.18 Here, as you can see, where the gray bars represent normal casein kinase 1 activity,
00:02:14.22 and the white bars represent the mutant casein kinase 1 activity.
00:02:19.16 You see, with five different substrates, the mutant enzymes showed reduced activity compared
00:02:25.22 to normal enzymes.
00:02:28.06 Now, for the mice that we generated to carry this specific human mutation, these mice
00:02:37.14 have a period length shorter than the control mice.
00:02:41.21 And this is as we expected, because we expect the phase-advanced animals should have
00:02:47.11 a shorter period length.
00:02:49.00 Now, if we remove the endogenous CK1 delta gene from the mutant transgene, then the period
00:02:56.12 is even shorter.
00:02:58.21 Now, interestingly, when we made Drosophila with this specific human mutation, we found that when
00:03:07.02 the flies carry mutant human CK1 delta their period is longer.
00:03:13.18 And it's longer than not only in the wild-type flies but also for the flies that carry wild-type
00:03:21.10 human CK1 delta gene.
00:03:23.13 So, what this told us is that, despite the fact that individual components of the molecular
00:03:30.25 clock are highly conserved between the mammalian system and Drosophila, it is likely that there
00:03:38.02 will be differences in the regulatory mechanism between these two different systems.
00:03:45.05 Now, one interesting feature for this particular family, as Louis mentioned, is that all the
00:03:53.18 mutation carriers for this family not only have a sleep behavior trait, they also all
00:04:00.08 have asthma and migraine headaches.
00:04:03.08 So, our hypothesis for this is that. we know that kinases can have up to
00:04:10.04 hundreds of different substrates.
00:04:12.09 So, if a mutation has occurred in a kinase, it is possible that the mutation can affect
00:04:20.11 more than one substrate, therefore lead to multiple phenotypes.
00:04:26.02 Now, because CK1 delta is very important for circadian regulation. so, we decided to
00:04:34.01 carry out the proteomic study for CK1 delta and also for CK1 epsilon.
00:04:39.28 And while we were doing this proteomic study, we decided to also address another question.
00:04:45.27 From previous studies, people have shown that casein kinase 1's. their activities remain
00:04:53.09 the same throughout the day.
00:04:56.00 So we wondered, can these kinases then phosphorylate different substrates at different times of
00:05:02.18 the day, therefore serving as part of their regular. regulatory function?
00:05:08.14 And indeed, our results show that CK1 delta and CK1 epsilon can phosphorylate
00:05:15.20 different substrates at different times of the day.
00:05:21.04 Now, from the proteomic study, we identified a novel gene called PHB2, here.
00:05:30.00 And PHB2 also plays an important role in circadian clock regulation.
00:05:35.26 PHB2 can suppress clock control genes' expression in a manner that is independent from BMAL
00:05:44.19 and CLOCK.
00:05:46.09 Interestingly, PHB2's protein level is regulated by CK1 epsilon.
00:05:53.15 But messenger RNA level of PHB2 is regulated by CK1 delta.
00:06:01.12 Now, the second mutation I want to tell you is for this particular family that Louis also
00:06:09.05 showed you.
00:06:10.05 We called it kindred 2174.
00:06:12.23 And this is the very first family that we collected.
00:06:16.12 The mutation carriers in this family also have four hours phase advance behavior trait.
00:06:22.23 Now, this is a very large family, so we were able to use this family and used a traditional
00:06:29.14 human genetics method to map the gene to the telomere region on the long arm of chromosome 2.
00:06:38.28 We then used a standard positional cloning method to find the mutation in the
00:06:44.23 Period 2 gene.
00:06:47.11 And it turns out the mutation was found in the amino acid position 662, that changes
00:06:54.23 from serine to glycine.
00:06:59.24 Now, when we examine the amino acid sequence in this serine 662 region, we found that the
00:07:07.25 amino acid sequence in this region is highly conserved among different PERs
00:07:13.25 from human and mice.
00:07:16.20 In addition, we found that there are four serine residues immediately C-terminal to
00:07:24.14 this serine 662, the first serine, here.
00:07:29.09 And interestingly, they all follow this exact serine-X-X-serine motif.
00:07:37.20 And serine-X-X-serine motif is a consensus sequence for casein kinase 1 activity.
00:07:45.26 So, we carried out a series of biochemical studies and what we found is that the
00:07:53.11 first serine of this five-serine region can be phosphorylated by a priming kinase.
00:08:01.08 And when this occurred then the following four serines can be phosphorylated by
00:08:07.22 casein kinase 1 delta.
00:08:11.03 Now, in the mouse model that we made to carry this specific PER2 serine 662 to glycine mutation,
00:08:21.27 the mutant transgenic mice have a period shorter than the wild-type mice, as we expected.
00:08:28.00 And this is also in agreement with the human subjects as a shorter period length.
00:08:33.03 Now, if we remove the endogenous PER2 allele from these mice, then the period became
00:08:40.01 even shorter.
00:08:41.21 Now, interestingly, when we generated the mouse model that changes the serine to an
00:08:49.13 aspartic acid to mimic the constitutive phosphoserine condition at this specific site,
00:08:58.14 then the transgenic mice have a longer period than the wild-type mice.
00:09:03.07 Now, again, if we remove the endogenous PER2 allele from serine to aspartic acid mutant
00:09:11.03 transgenic mice, their period became longer.
00:09:16.27 So, what we have here is that with this five-serine region the first serine is phosphorylated
00:09:24.20 by a priming kinase.
00:09:26.14 And then CK1 delta then phosphorylates the four additional serines.
00:09:31.00 And when this happens, then the animals will have a longer period, which we can think of it
00:09:36.06 as a slower clock, because it takes longer to finish the cycle.
00:09:41.09 Now, if the first serine is blocked, it cannot be phosphorylated, therefore none of them
00:09:48.09 are phosphorylated, then the animal will have a shorter period.
00:09:53.15 And we can think of this as a faster clock.
00:09:56.10 Now, when we look at the activity recording for our serine to glycine mutant transgenic mice,
00:10:04.09 we found that four hours before we turn the light off the animal starts to become
00:10:11.17 active.
00:10:12.17 The activity turned on.
00:10:15.16 And four hours before the light on, the activity starts to wind down.
00:10:21.08 And this is very similar to human subjects with four hours phase advance.
00:10:25.15 So, this mouse model actually recapitulates the human phenotype very well.
00:10:32.20 So, we showed that this serine to glycine mutation will make the PER2 protein
00:10:41.06 become hypophosphorylated.
00:10:43.20 But how does a hypophosphorylated PER2 then lead to an advanced sleep phase behavior trait?
00:10:50.24 Well, there were three obvious possibilities.
00:10:54.22 First is that the mutation could affect PER's protein stability.
00:10:59.21 Second is that the mutation will affect PER2's nuclear translocation timing or mechanism.
00:11:06.11 Third is that a mutation could affect PER2's repressor activity,
00:11:12.09 therefore change the transcriptional regulation.
00:11:15.17 And we examined each of these possibilities.
00:11:19.05 And our results show that the major effect for this mutation is changing PER2's
00:11:25.23 repressor activity.
00:11:27.10 Now, here you can see that the wild-type PER2 messenger RNA, peaked as. here, this peak.
00:11:38.07 And the SG PER2 messenger RNA actually peaked earlier than the wild-type PER2 messenger RNA.
00:11:46.15 And the SD PER2 messenger RNA peaked later than the wild-type, agreeing with. that
00:11:52.28 SG has a shorter period length and advanced sleep behavior trait.
00:11:58.14 Now, not only that the SG PER2 messenger RNA peaked lower than the wild-type PER2 messenger
00:12:06.26 and the peak for SD PER2 is higher than the wild-type PER2, and this is true not only
00:12:14.24 for the mouse endogenous PER2 messenger RNA, also for human PER2 transgene messenger RNA.
00:12:22.11 So, what this result told us is that the SG PER2 is a stronger repressor than the wild-type protein,
00:12:30.10 and the SD PER2 is a weaker repressor than the wild-type PER2 protein.
00:12:38.14 So, we knew that PER2 protein is regulated by casein kinase 1 delta, so we wondered whether
00:12:47.23 we could use our mouse model to study genetic interaction between CK1 delta and PER2.
00:12:55.18 And this slide is just to show you that the copy number of CK1 delta actually does not
00:13:02.10 affect mouse period length.
00:13:05.23 With the heterozygous CK1 delta knockout mice with only one copy of the normal gene and
00:13:15.00 CK1 delta wild-type transgene with 4-5 copies of the normal gene, their period remains the
00:13:21.25 same with wild-type mice.
00:13:24.09 Again for the serine to glycine PER2 mutant transgene, the period is shorter than the
00:13:31.05 wild-type mice.
00:13:33.08 But if we cross these SG mutant transgenic mice with the CK1 delta heterozygous knockout mice,
00:13:41.14 their period became longer.
00:13:43.28 Now, if we cross the SG mutant transgenic mice with the CK1 delta wild-type transgene,
00:13:51.19 then the period became shorter.
00:13:54.03 So, what this result told us is that on PER2 protein, in addition to this
00:14:03.05 phosphorylation site by CK1 delta around 662, there are other CK1 delta phosphorylation sites for PER2.
00:14:12.03 And these other sites, when they are phosphorylated, they can lead to a shorter period length.
00:14:18.09 So, we proposed this model to explain all of our data together.
00:14:24.15 We think that PER2 has multiple phosphorylation sites by casein kinase 1 delta.
00:14:30.14 And one of these sites is around serine 662.
00:14:33.25 And then. when this site is phosphorylated, it can lead to increased PER2 messenger RNA
00:14:41.06 and protein, and lead to a longer period length.
00:14:45.08 Now, when these other sites are phosphorylated, it can lead to increased PER2 degradation,
00:14:52.22 therefore lower PER2 protein level.
00:14:55.15 This then leads to a shorter period length.
00:14:58.03 And under normal conditions, these different pathways have to maintain a delicate balance
00:15:03.15 in order for the animals to have a stable, normal period length.
00:15:08.25 So, all these results really point out the importance of PER2 phosphorylation in setting
00:15:15.28 the speed of the clock.
00:15:18.14 In fact, this is true not only for PER2 protein but also for other clock proteins as well.
00:15:26.19 So, then this, then, raised another question, which is, are other post-translational modifications
00:15:34.15 also important for regulating the circadian clock?
00:15:39.26 So, as I showed you earlier, we did a proteomic study for CK1 delta.
00:15:48.21 And GSK3 beta is another important kinase for circadian regulation.
00:15:54.24 So, we also did a proteomic study for GSK3 beta.
00:16:00.04 In this proteomic study, we found more than 400 potential GSK3 beta substrates.
00:16:06.24 And these more than 400 proteins can be mapped onto many biological pathways, including some
00:16:13.07 of them previously shown and others are novel biological pathways for GSK3 beta.
00:16:22.25 Out of these more than 400 proteins, we decided to follow up on one particular protein, which
00:16:29.18 is O-GlcNAc transferase, or OGT in short.
00:16:35.22 OGT and OGA, which is O-GlcNAcase, they are responsible for the O-GlcNAc post-translational
00:16:44.06 modification for proteins.
00:16:49.17 Interestingly, the GSK3 beta phosphorylation can significantly increase OGT's activity,
00:16:58.01 here, where the phosphorylation by GSK3 beta significantly increases the activity.
00:17:06.00 Now, O-GlcNAc modification also occurs on serine and threonine.
00:17:11.10 So, the first question we asked was, does O-GlcNAcylation also play a role in regulating
00:17:18.17 the circadian clock?
00:17:21.23 We first used an in vitro system to see if O-GlcNAcylation can affect circadian period length.
00:17:31.12 When we add OGA inhibitor to the cells, we found that the period length becomes longer.
00:17:38.21 Now, if we add OGT inhibitor to the cells, then the period became shorter.
00:17:46.26 We also confirmed this in vivo.
00:17:50.00 With OGT conditional knockout mice, we found that their period is shorter than the control mice.
00:17:58.02 For the Drosophila, the OGT knockdown, the period is shorter.
00:18:05.13 The OGA knockdown, the period is longer than the wild-type fly.
00:18:10.04 So, all these different systems suggest that under higher O-GlcNAcylation conditions,
00:18:17.15 it can lead to a longer period length.
00:18:20.10 And the lower O-GlcNAcylation level leads to a shorter period length.
00:18:28.23 We then found that at least two of the core clock components are modified by O-GlcNAc.
00:18:35.25 CLOCK protein, when it's modified by the O-GlcNAc, it actually reduced its transcription activity.
00:18:43.22 But the PER2 protein, when it's modified by O-GlcNAc, it actually further enhanced its
00:18:51.19 repressor activity.
00:18:53.05 Now, with PER2 luciferase activity as an index, we see that CLOCK and BMAL can turn on PER2 promoter.
00:19:04.04 In the presence of OGT, the transcription activity is significantly suppressed.
00:19:11.07 Now, wild-type PER2 protein is a repressor for CLOCK and BMAL activity.
00:19:18.16 In the presence of OGT, the PER2's repressor activity is further enhanced.
00:19:24.07 Now, as I told you earlier, the PER2 S to G mutant is a stronger repressor than the
00:19:33.26 wild-type protein.
00:19:35.19 However, when we add OGT to the reaction with mutant PER2 protein, it did not affect
00:19:43.21 the transcription activity.
00:19:46.06 This then gave us an idea that maybe O-GlcNAc modification plays a role on this serine 662 site.
00:19:55.09 We used a culture system, together with western blot, to show that when PER2 protein
00:20:02.13 is O-GlcNAc modified it actually blocks the phosphorylation at serine 662 site.
00:20:09.16 And also, if the serine 662 of PER2 is phosphorylated, the PER2 protein does not get O-GlcNAc modified
00:20:18.15 as well as the PER2 protein that is not phosphorylated at serine 662.
00:20:24.00 So, together, these results suggest that there is an interplay between O-GlcNAcylation and
00:20:31.10 phosphorylation at PER2 serine 662.
00:20:37.17 We also used mass spectrometry to map all the O-GlcNAc modification sites,
00:20:44.16 focusing on the serine 662 region.
00:20:47.05 And we found many O-GlcNAc modification sites, marked in red here, including the serine 662,
00:20:55.21 serine 668, and serine 671.
00:21:01.17 Now, OGT and OGA are responsible for O-GlcNAc modification of the protein.
00:21:09.03 And O-GlcNAcylation is dependent on its substrate, UDP-GlcNAc.
00:21:15.22 UDP-GlcNAc is derived from nutrients, including glucose, amino acids, and nucleic acids, through
00:21:24.26 hexosamine biosynthetic pathways.
00:21:27.24 Now, O-GlcNAcylation can regulate circadian rhythm.
00:21:32.13 So, we then wondered, well, can glucose level modulate the circadian clock?
00:21:41.00 So, we did this simple experiment.
00:21:44.11 Here, under low glucose concentration, we found that the serine 662 region of the PER2
00:21:52.25 can be phosphorylated as long as CK1 delta is present, regardless of if OGT or OGA
00:22:00.12 is there or not.
00:22:02.04 However, under high glucose concentration, the phosphorylation in this region is blocked
00:22:10.00 as long as OGT and OGA is there, regardless of if CK1 delta is there or not.
00:22:17.03 In summary, we found that in this serine 662 region there are five serines in a row.
00:22:23.13 When the first serine is phosphorylated by a priming kinase, therefore the four additional
00:22:29.26 serines are phosphorylated by CK1 delta.
00:22:33.07 This then leads to a longer period for the animal.
00:22:38.06 Under high glucose concentration, the O-GlcNAcylation can take over and block the phosphorylation
00:22:44.24 for this region, therefore leading to a shorter period and a faster clock.
00:22:49.28 And we call this "clock sugar rush".
00:22:54.20 So, we have so far collected more than 90 advanced sleep phase families.
00:23:01.13 And we are continuing to use these families to identify genes and mutations responsible
00:23:07.16 for this behavior trait.
00:23:10.02 When we find genes and mutations, we study their protein functions.
00:23:13.27 At the same time, we also generate mouse and fly models
00:23:18.12 to help us understand the molecular mechanism.
00:23:21.25 And with this parallel approach, we hope to gain a better understanding of human circadian
00:23:28.08 and sleep mechanisms.
00:23:30.12 With a better understanding of these regulatory mechanisms, we'll be able to come up with
00:23:35.25 a better therapeutic intervention for sleep-related disorders.
00:23:43.02 I want to acknowledge my long-term collaborators, Louis Ptacek and Chris Jones.
00:23:48.00 And also all the people who contributed to this work.

  • Part 1: Connections between Clock and other Phenotypes

Improve Sleep: Tips to Improve Your Sleep When Times Are Tough

Just like food or water, sleep is a biological necessity for life and health. Research shows that the hours we spend sleeping are incredibly important and far from passive. During sleep, your body is busy fighting off viruses and other pathogens, operating a waste removal system to clean the brain, looking for cancer cells and getting rid of them, repairing injured tissues, and forming vital memories that are essential for learning. Getting enough sleep can improve mental health, mood, and ability to think and make good decisions. It is important for the functioning of our heart and other organs.

Most adults need 7 or more hours of good quality (uninterrupted) sleep each day. Some may need even more.

Adequate high-quality sleep is especially important during stressful times. To help you adapt to quickly evolving demands and changes in your personal and work life during the COVID-19 outbreak, the following evidence-based suggestions can help improve your sleep.

Set aside enough time for sleep.

Give yourself enough time in bed to get the amount of sleep you need to wake up feeling well rested. This varies from person to person, but most healthy adults need 7 or more hours of sleep.

Consistent sleep times improve sleep.

Go to bed and get up at about the same times every day, including days off. Ideally, you should go to bed early enough that you don’t need an alarm to wake up.

Exercise improves sleep.

During the day, get some exercise. Even a 10-minute walk will improve sleep, and more is better. Plan on finishing exercise at least 3 hours before sleep is planned.

Bright light during the daytime helps.

Getting bright light during the daytime strengthens your biological rhythms that promote alertness during work and sleep at the end of your day. So, during the daytime spend 30 minutes or so outside in the sunlight. Getting bright light during the first hours of your day is particularly helpful. Even time spent outside on a cloudy day is better than exclusive exposure to dim indoor light. If you can’t get outside, spend time in a brightly lit indoor area.

Where you sleep matters.

Have a good sleep environment that is very dark, quiet, cool, and comfortable.

  • Make the bedroom very dark, blocking out any lights in the room (especially blue and white lights). Cover the windows with opaque window covering if necessary. Use an eye mask if it’s hard to avoid lights from traffic or streetlamps.
  • Use soft ear plugs if your sleep environment is noisy.
  • Have a comfortably cool room temperature—about 65º to 68º F for most of us—and use covers.
  • Have a comfortable mattress and pillow.
  • Do not let pets or phones disturb your sleep.

Use your sleep space for only two things.

To condition your brain to relax when you go into the bedroom, use it only for sleep and intimacy. Do not watch TV, read, or work in the bedroom.

Prepare for a good night’s sleep about 1.5 hours before bedtime.

Follow a relaxing routine 1.5 hours before bedtime to help your body make the transition from being awake to falling asleep. Consider setting an alarm 1.5 hours before bedtime to start preparing for sleep. Don’t expose your eyes to computer or phone screens. Avoid excitement like watching an action movie or reading upsetting news stories. Brushing your teeth, washing your face, and getting into a pre-sleep routine will help you relax. Transition to dim lighting during this time (for example, don’t use a bright light in the bathroom).

Try relaxation techniques.

  • View tips from the Dartmouth Wellness Center.
  • Taking a warm bath 30 minutes to 2 hours before bedtime can help promote relaxation and optimize body temperature changes that aid in sleep.

Check your intake.

  • Avoid heavy or spicy meals 3 hours before your regular bedtime.
  • Limit liquids several hours before sleep to avoid having to get up to go to the bathroom.
  • Avoid alcohol near bedtime. It may help you fall asleep but can cause sleep disturbances. If you plan to drink alcohol, finish several hours before bedtime.
  • Avoid caffeine, chocolate, and nicotine for 5 or more hours before sleep is planned—more if you are sensitive.

Pay attention to your body’s cues. If you get very sleepy earlier than usual, then by all means, go to bed. This will allow extra time for sleep. Drowsiness is your body’s way of saying that you need sleep. Your body may be fighting off an infection or needing extra sleep to recover from what happened during the day. Researchers theorize that sleep and the immune system work together to fight off viruses and other pathogens. Your body also needs more sleep after experiencing high mental or physical demands.

What if these suggestions don’t work?

It may be wise to get help. Call your doctor if you spend 7 to 9 hours in bed but:

  • You consistently take 30 minutes or more to fall asleep.
  • You consistently awaken several times during sleep or for long periods.
  • You take frequent naps.
  • You often feel sleepy, especially at inappropriate times.

Getting enough good quality sleep significantly improves our health and safety, as well as our ability to perform on the job. As a result, promoting sleep health and an alert workforce is in the interest of managers, workers, and the consumers of the organization’s goods and services. Please share steps your employer has taken that makes it possible for you to use these sleep tips in your daily life.

This is a part of the series of blogs sponsored by NIOSH’s Healthy Work Design and Well-Being Program on issues impacted by the COVID-19 pandemic. Other blogs include:

Claire C Caruso PhD, RN, FAAN, Research Health Scientist

L. Casey Chosewood, MD, MPH, Director, Office for Total Worker Health®


Stages 1-2

As we fall into sleep, our brain stays active and fires into its editing process—deciding which memories to keep and which ones to toss.

The initial transformation happens quickly. The human body does not like to stall between states, lingering in doorways. We prefer to be in one realm or another, awake or asleep. So we turn off the lights and lie in bed and shut our eyes. If our circadian rhythm is pegged to the flow of daylight and dark, and if the pineal gland at the base of our brain is pumping melatonin, signaling it’s nighttime, and if an array of other systems align, our neurons swiftly fall into step.

Neurons, some 86 billion of them, are the cells that form the World Wide Web of the brain, communicating with each other via electrical and chemical signals. When we’re fully awake, neurons form a jostling crowd, a cellular lightning storm. When they fire evenly and rhythmically, expressed on an electroencephalogram, or EEG, by neat rippled lines, it indicates that the brain has turned inward, away from the chaos of waking life. At the same time, our sensory receptors are muffled, and soon we’re asleep.

Scientists call this stage 1, the shallow end of sleep. It lasts maybe five minutes. Then, ascending from deep in the brain, comes a series of electric sparks that zap our cerebral cortex, the pleated gray matter covering the outer layer of the brain, home of language and consciousness. These half-second bursts, called spindles, indicate that we’ve entered stage 2.

Our brains aren’t less active when we sleep, as was long thought, just differently active. Spindles, it’s theorized, stimulate the cortex in such a way as to preserve recently acquired information—and perhaps also to link it to established knowledge in long-term memory. In sleep labs, when people have been introduced to certain new tasks, mental or physical, their spindle frequency increases that night. The more spindles they have, it seems, the better they perform the task the next day.

The strength of one’s nightly spindles, some experts have suggested, might even be a predictor of general intelligence. Sleep literally makes connections you might never have consciously formed, an idea we’ve all intuitively realized. No one says, “I’m going to eat on a problem.” We always sleep on it.

The Japanese term inemuri, or “sleeping while present,” is a distinct form of napping in which a person dozes in a place not meant for sleep, such as the subway—or even at a dinner party or the office. “Since you’re officially not sleeping,” says Brigitte Steger, a Japan specialist at the University of Cambridge in England, “to be socially acceptable you should behave as is appropriate in a certain situation. For example in a meeting, you half pretend to be listening or hide your sleeping head behind paperwork.” If you’re not already known as a slacker, Steger adds, a little inemuri may even enhance your business reputation: It demonstrates that you’re working yourself to exhaustion.

The waking brain is optimized for collecting external stimuli, the sleeping brain for consolidating the information that’s been collected. At night, that is, we switch from recording to editing, a change that can be measured on the molecular scale. We’re not just rotely filing our thoughts—the sleeping brain actively curates which memories to keep and which to toss.

It doesn’t necessarily choose wisely. Sleep reinforces our memory so powerfully—not just in stage 2, where we spend about half our sleeping time, but throughout the looping voyage of the night—that it might be best, for example, if exhausted soldiers returning from harrowing missions did not go directly to bed. To forestall post-traumatic stress disorder, the soldiers should remain awake for six to eight hours, according to neuroscientist Gina Poe at the University of California, Los Angeles. Research by her and others suggests that sleeping soon after a major event, before some of the ordeal is mentally resolved, is more likely to turn the experience into long-term memories.

Stage 2 can last up to 50 minutes during the night’s first 90-minute sleep cycle. (It typically occupies a smaller portion of subsequent cycles.) Spindles can arrive every few seconds for a while, but when these eruptions taper off, our heart rate slows. Our core temperature drops. Any remaining awareness of the external environment disappears. We commence the long dive into stages 3 and 4, the deep parts of sleep.


Brain Chemicals That Cause Sleep Paralysis Discovered

During the most dream-filled phase of sleep, our muscles become paralyzed, preventing the body from acting out what's going on in the brain. Now, researchers have discovered the brain chemicals that keep the body still in sleep.

The findings could be helpful for treating sleep disorders, the scientists report Wednesday (July 18) in The Journal of Neuroscience.

The brain chemicals kick into action during rapid eye movement (REM) sleep, a phase that usually begins about 90 minutes into a night's rest. During REM, the brain is very active, and dreams are at their most intense. But the voluntary muscles of the body &mdash arms, legs, fingers, anything that is under conscious control &mdash are paralyzed.

This paralysis keeps people still even as their brains are acting out fantastical scenarios it's also the reason people sometimes experience sleep paralysis, or the experience of waking up while the muscles are still frozen. This sensation has been the basis for myths such as the succubus and the incubus, demons said to pin people down in their sleep, usually to have sex with them. [Top 10 Spooky Sleep Disorders]

The chemistry of sleep

Exactly how the muscles are paralyzed has been a mystery, however. Early studies pegged a neurotransmitter called glycine as the culprit, but paralysis still occurred even when the receptors that read glycine's presence were blocked, disproving that notion.

So University of Toronto researchers Patricia Brooks and John Peever cast a wider net. They focused on two different nerve receptors in the voluntary muscles, one called metabotropic GABAB and one called ionotropic GABAA/glycine. The latter receptor responds to both glycine and a different communication chemical called gamma-aminobutyric acid, or GABA, while the first responds to GABA and not glycine.

The researchers used drugs to "switch off" these receptors in rats and discovered that the only way to prevent sleep paralysis during REM was to shut both types off at the same time. What that means is that glycine alone isn't enough to paralyze the muscles. You need GABA, too.

Treating sleep disorders

Understanding this alphabet soup of neurotransmitters is important for people who have sleep disorders, especially an odd condition called REM behavior disorder. In this disorder, people don't become paralyzed during REM sleep. That means they act out their dreams, talking, thrashing and even punching or hitting in their sleep.

Currently, Clonazepam, an antipsychotic drug, is used to treat REM behavior disorder. The new study could point to new treatments for the problem, sleep researcher Dennis McGinty of the University of California, Los Angeles, who was not involved in the study, said in a statement. The researchers hope that the results could help explain the link between REM behavior disorder and more deadly conditions.

"Understanding the precise mechanism behind these chemicals&rsquo role in REM sleep disorder is particularly important because about 80 percent of people who have it eventually develop a neurodegenerative disease, such as Parkinson&rsquos disease," Peever said. "REM sleep behavior disorder could be an early marker of these diseases, and curing it may help prevent or even stop their development."


Why Do We Dream? A New Theory on How It Protects Our Brains

W hen he was two years old, Ben stopped seeing out of his left eye. His mother took him to the doctor and soon discovered he had retinal cancer in both eyes. After chemotherapy and radiation failed, surgeons removed both his eyes. For Ben, vision was gone forever.

But by the time he was seven years old, he had devised a technique for decoding the world around him: he clicked with his mouth and listened for the returning echoes. This method enabled Ben to determine the locations of open doorways, people, parked cars, garbage cans, and so on. He was echolocating: bouncing his sound waves off objects in the environment and catching the reflections to build a mental model of his surroundings.

Echolocation may sound like an improbable feat for a human, but thousands of blind people have perfected this skill, just like Ben did. The phenomenon has been written about since at least the 1940s, when the word &ldquoecholocation&rdquo was first coined in a Science article titled &ldquoEcholocation by Blind Men, Bats, and Radar.&rdquo

How could blindness give rise to the stunning ability to understand the surroundings with one&rsquos ears? The answer lies in a gift bestowed on the brain by evolution: tremendous adaptability.

Whenever we learn something new, pick up a new skill, or modify our habits, the physical structure of our brain changes. Neurons, the cells responsible for rapidly processing information in the brain, are interconnected by the thousands&mdashbut like friendships in a community, the connections between them constantly change: strengthening, weakening, and finding new partners. The field of neuroscience calls this phenomenon &ldquobrain plasticity,&rdquo referring to the ability of the brain, like plastic, to assume new shapes and hold them. More recent discoveries in neuroscience suggest that the brain&rsquos brand of flexibility is far more nuanced than holding onto a shape, though. To capture this, we refer to the brain&rsquos plasticity as &ldquolivewiring&rdquo to spotlight how this vast system of 86 billion neurons and 0.2 quadrillion connections rewires itself every moment of your life.

Neuroscience used to think that different parts of the brain were predetermined to perform specific functions. But more recent discoveries have upended the old paradigm. One part of the brain may initially be assigned a specific task for instance, the back of our brain is called the &ldquovisual cortex&rdquo because it usually handles sight. But that territory can be reassigned to a different task. There is nothing special about neurons in the visual cortex: they are simply neurons that happen to be involved in processing shapes or colors in people who have functioning eyes. But in the sightless, these same neurons can rewire themselves to process other types of information.

Mother Nature imbued our brains with flexibility to adapt to circumstances. Just as sharp teeth and fast legs are useful for survival, so is the brain&rsquos ability to reconfigure. The brain&rsquos livewiring allows for learning, memory, and the ability to develop new skills.

In Ben&rsquos case, his brain&rsquos flexible wiring repurposed his visual cortex for processing sound. As a result, Ben had more neurons available to deal with auditory information, and this increased processing power allowed Ben to interpret soundwaves in shocking detail. Ben&rsquos super-hearing demonstrates a more general rule: the more brain territory a particular sense has, the better it performs.

Recent decades have yielded several revelations about livewiring, but perhaps the biggest surprise is its rapidity. Brain circuits reorganize not only in the newly blind, but also in the sighted who have temporary blindness. In one study, sighted participants intensively learned how to read Braille. Half the participants were blindfolded throughout the experience. At the end of the five days, the participants who wore blindfolds could distinguish subtle differences between Braille characters much better than the participants who didn&rsquot wear blindfolds. Even more remarkably, the blindfolded participants showed activation in visual brain regions in response to touch and sound. When activity in the visual cortex was temporarily disrupted, the Braille-reading advantage of the blindfolded participants went away. In other words, the blindfolded participants performed better on the touch-related task because their visual cortex had been recruited to help. After the blindfold was removed, the visual cortex returned to normal within a day, no longer responding to touch and sound.

But such changes don&rsquot have to take five days that just happened to be when the measurement took place. When blindfolded participants are continuously measured, touch-related activity shows up in the visual cortex in about an hour.

What does brain flexibility and rapid cortical takeover have to do with dreaming? Perhaps more than previously thought. Ben clearly benefited from the redistribution of his visual cortex to other senses because he had permanently lost his eyes, but what about the participants in the blindfold experiments? If our loss of a sense is only temporary, then the rapid conquest of brain territory may not be so helpful.

And this, we propose, is why we dream.

In the ceaseless competition for brain territory, the visual system has a unique problem: due to the planet&rsquos rotation, all animals are cast into darkness for an average of 12 out of every 24 hours. (Of course, this refers to the vast majority of evolutionary time, not to our present electrified world.) Our ancestors effectively were unwitting participants in the blindfold experiment, every night of their entire lives.

So how did the visual cortex of our ancestors&rsquo brains defend its territory, in the absence of input from the eyes?

We suggest that the brain preserves the territory of the visual cortex by keeping it active at night. In our &ldquodefensive activation theory,&rdquo dream sleep exists to keep neurons in the visual cortex active, thereby combating a takeover by the neighboring senses. In this view, dreams are primarily visual precisely because this is the only sense that is disadvantaged by darkness. Thus, only the visual cortex is vulnerable in a way that warrants internally-generated activity to preserve its territory.

In humans, sleep is punctuated by rapid eye movement (REM) sleep every 90 minutes. This is when most dreaming occurs. (Although some forms of dreaming can occur during non-REM sleep, such dreams are abstract and lack the visual vividness of REM dreams.)

REM sleep is triggered by a specialized set of neurons that pump activity straight into the brain&rsquos visual cortex, causing us to experience vision even though our eyes are closed. This activity in the visual cortex is presumably why dreams are pictorial and filmic. (The dream-stoking circuitry also paralyzes your muscles during REM sleep so that your brain can simulate a visual experience without moving the body at the same time.) The anatomical precision of these circuits suggests that dream sleep is biologically important&mdashsuch precise and universal circuitry rarely evolves without an important function behind it.

The defensive activation theory makes some clear predictions about dreaming. For example, because brain flexibility diminishes with age, the fraction of sleep spent in REM should also decrease across the lifespan. And that&rsquos exactly what happens: in humans, REM accounts for half of an infant&rsquos sleep time, but the percentage decreases steadily to about 18% in the elderly. REM sleep appears to become less necessary as the brain becomes less flexible.

Of course, this relationship is not sufficient to prove the defensive activation theory. To test it on a deeper level, we broadened our investigation to animals other than humans. The defensive activation theory makes a specific prediction: the more flexible an animal&rsquos brain, the more REM sleep it should have to defend its visual system during sleep. To this end, we examined the extent to which the brains of 25 species of primates are &ldquopre-programmed&rdquo versus flexible at birth. How might we measure this? We looked at the time it takes animals of each species to develop. How long do they take to wean from their mothers? How quickly do they learn to walk? How many years until they reach adolescence? The more rapid an animal&rsquos development, the more pre-programmed (that is, less flexible) the brain.

As predicted, we found that species with more flexible brains spend more time in REM sleep each night. Although these two measures&mdashbrain flexibility and REM sleep&mdashwould seem at first to be unrelated, they are in fact linked.

As a side note, two of the primate species we looked at were nocturnal. But this does not change the hypothesis: whenever an animal sleeps, whether at night or during the day, the visual cortex is at risk of takeover by the other senses. Nocturnal primates, equipped with strong night vision, employ their vision throughout the night as they seek food and avoid predation. When they subsequently sleep during the day, their closed eyes allow no visual input, and thus, their visual cortex requires defense.

Dream circuitry is so fundamentally important that it is found even in people who are born blind. However, those who are born blind (or who become blind early in life) don&rsquot experience visual imagery in their dreams instead, they have other sensory experiences, such as feeling their way around a rearranged living room or hearing strange dogs barking. This is because other senses have taken over their visual cortex. In other words, blind and sighted people alike experience activity in the same region of their brain during dreams they differ only in the senses that are processed there. Interestingly, people who become blind after the age of seven have more visual content in their dreams than those who become blind at younger ages. This, too, is consistent with the defensive activation theory: brains become less flexible as we age, so if one loses sight at an older age, the non-visual senses cannot fully conquer the visual cortex.

If dreams are visual hallucinations triggered by a lack of visual input, we might expect to find similar visual hallucinations in people who are slowly deprived of visual input while awake. In fact, this is precisely what happens in people with eye degeneration, patients confined to a tank-respirator, and prisoners in solitary confinement. In all of these cases, people see things that are not there.

We developed our defensive activation theory to explain visual hallucinations during extended periods of darkness, but it may represent a more general principle: the brain has evolved specific circuitry to generate activity that compensates for periods of deprivation. This might occur in several scenarios: when deprivation is regular and predictable (e.g., dreams during sleep), when there is damage to the sensory input pathway (e.g., tinnitus or phantom limb syndrome), and when deprivation is unpredictable (e.g., hallucinations induced by sensory deprivation). In this sense, hallucinations during deprivation may in fact be a feature of the system rather than a bug.

We&rsquore now pursuing a systematic comparison between a variety of species across the animal kingdom. So far, the evidence has been encouraging. Some mammals are born immature, unable to regulate their own temperature, acquire food, or defend themselves (think kittens, puppies, and ferrets). Others are born mature, emerging from the womb with teeth, fur, open eyes, and the abilities to regulate their temperature, walk within an hour of birth, and eat solid food (think guinea pigs, sheep, and giraffes). The immature animals have up to 8 times more REM sleep than those born mature. Why? Because when a newborn brain is highly flexible, the system requires more effort to defend the visual system during sleep.

Since the dawn of communication, dreams have perplexed philosophers, priests, and poets. What do dreams mean? Do they portend the future? In recent decades, dreams have come under the gaze of neuroscientists as one of the field&rsquos central unsolved mysteries. Do they serve a more practical, functional purpose? We suggest that dream sleep exists, at least in part, to prevent the other senses from taking over the brain&rsquos visual cortex when it goes unused. Dreams are the counterbalance against too much flexibility. Thus, although dreams have long been the subject of song and story, they may be better understood as the strange lovechild of brain plasticity and the rotation of the planet.


Take Out the Trash

That’s what scientists think REM does. It helps your brain clear out information you don’t need. People who take a look at a hard puzzle solve it more easily after they sleep than before. And they remember facts and tasks better, too. Those deprived of REM in particular -- compared with other sleep stages -- lose this advantage.


If you just fall fast asleep – the way we all wish we could – you’re not going to remember anything from that part of your sleep cycle – Robert Stickgold

Stickgold says that a lot of people remember their dreams from a sleep onset period, when the mind starts wandering and dreamlike imagery occurs as people drift in and out of sleep – a process called “hypnagogic dreaming”. Stickgold says he carried out a study some years ago where students in a lab were awoken shortly after they started entering this state. “Every last one of them remembered dreaming,” he says.

“This stage is the first five or 10 minutes after falling asleep. If you just fall fast asleep – the way we all wish we could – you’re not going to remember anything from that part of your sleep cycle.”

Often we are startled out of our slumber by an alarm clock, which makes it harder for us to remember our dreams (Credit: Emmanuel Lafont)

So what if you actively want to remember your dreams? Obviously, each sleeper is different, but there are some general tips which might help you to hold on to your dreams.

“Dreams are incredibly fragile when we first wake up, and we don’t really have an answer for why that is,” says Stickgold. “If you’re the kind of person who leaps up out of bed and goes about their day, you’re not going to remember your dreams. When you sleep in on a Saturday or Sunday morning, that’s an excellent time to remember dreams.

“What I tell my students on my courses is, when you wake up, try to lie still – don’t even open your eyes. Try to ‘float’ and at the same time try to remember what was in your dream. What you’re doing is you’re reviewing dreams as you enter your waking state and you’ll remember them just like any other memory.”

There are even more surefire ways to remember dreams, Stickgold says. “I tell people to drink three big glasses of water before they go to bed. Not three glasses of beer, because alcohol in an REM suppressant, but water. You’ll wake up three or four times in the night and you’ll tend to wake up at the end of an REM cycle of sleep which is natural.”

And there is another piece of advice offered by some sleep researchers – that simply repeating to yourself as you drift towards sleep that you want to remember your dreams means you wake remembering them. Stickgold laughs. “It actually works. If you do that you really are going to remember more dreams, it’s like saying ‘There’s no place like home’. It really works.”


Watch the video: The Sense of Touch - Senses for Kids (January 2022).