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How Do We Wake Up? The Processes Behind It

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Waking up can be linked to various reasons, so to speak. One of them is in the morning when the light hits our eyes. We can also wake up due to the cat breaking a vase or loud music playing. We can also wake up in the middle of the night feeling fully rested.

Different processes occur in our body for each of those situations. Scientists have recently managed to find the individual genes that influence our circadian rhythm and nerve cells that wake us up.

Circadian rhythm and how the body prepares to wake up

The internal clock of our body is called the circadian rhythm. In the brain – in the hypothalamus, there is a particular group of cells which keeps track of the time through genetic instructions and hormones. These specialized time-keeping cells are known as Suprachiasmatic nucleus (SCN).

SCN relies on natural daylight. Throughout the day, hormones and neurotransmitters ebb and flow – the process which does both – it keeps us alert and energetic and increases sleep propensity (need for sleep). In the morning, melatonin levels are low and dopamine is high, which is why most people feel more energy in the first half of the day. As the evening approaches, it’s the opposite – melatonin rises and dopamine drops. Melatonin is a hormone which makes us sleepy and is directly influenced by light.

The body temperature starts increasing and every muscle gets slowly ‘awaken’, or ready for action. Finally, when all systems are go, we wake up.

Our circadian clock also regulates hunger, time for performing our daily activities, and energy levels. Today, many people live with a confused, out-of-tune circadian rhythm due to irregular sleep-wake schedules (sleeping too little in the week and ‘making up’ for it by sleeping in on the weekends), irregular meal time, and let’s not forget the negative effect of the artificial lights.

This is why many people have poor sleep quality and are unable to wake up with the morning light. Alarm clocks, if not used every day at the same time, can make things worse, because a person can be woken up from the deep sleep, feeling groggy for up to several hours.

How the light wakes us up

As the morning light hits our eyelids, although closed, our eyes register light (through rod and cone receptors). The information about the day travels to the hypothalamus. Hypothalamus, in turn, responds by instructing the glands in our body to inhibit melatonin production and increase wakefulness hormones, like cortisol. The process continues to trigger other wakeup mechanisms described above.

Even when we sleep in through the morning, our eyes still register light, and that kind of sleep is not as restorative. Therefore, we need both – darkness throughout the night and light in the morning for a good night’s rest and the process of gradual waking up.

How external stimuli (sounds and touch) wake us up

If there is a sound while we sleep, our brain (auditory cortex) will process it and react to it – as can be seen on EEG recordings. However, in order to keep us asleep, the sounds we hear are distorted in the nerve cells and the incomplete, weakened information reaches the auditory cortex, so the response from it is weak, and our sleep continuity is uninterrupted.

The process of distorting the external stimuli is associated with certain types of brain waves known as sleep spindles. Thanks to them, we are a lot less responsive to our environment. Sleep spindles occur throughout the NREM (non-rapid eye movement) sleep.

However, the spindles are only so powerful in stimulus distortion. If a sound is too strong, the auditory cortex will receive the information and respond to it through arousal.

The same process goes for touch, except that this type of information reaches the somatosensory cortex.

Stimulus distortion allows us to sleep through unimportant stimuli, like the fridge and traffic noise, or a fly that landed on our hand. However, stronger stimulus suggests the possibility of danger and is not ‘cut out’ of our perception.

REM sleep and waking up

Some scientists hypothesize that one of the roles of the rapid eye movement sleep is to prepare to wake up the body. Although during REM we experience muscle atonia (inability to move the body), the internal processes are changing – the brain activity increases and brain waves become similar to those of a wakeful state. The body temperature rises, breathing speeds up. Most instances of waking up at night or in the morning (naturally, not with an alarm clock) are from the REM sleep. We know for sure that people experience more REM in the second half of the night and that the REM episodes increase as the wake-up time approaches.

Neurons and genes behind the wakeup process

The flip-flop switch

Numerous research has been conducted in order to discover the underlying processes of waking up. Scientists know about the ‘flip-flop’ switch which turns on when we wake up, and off when we fall asleep. This switch consists of two poles – sleep-promoting, which inhibits wakefulness neurons and processes, and a wakefulness-promoting pole, which also works by inhibiting the opposite.

The switch ensures we remain in one state and not just fall asleep or wake up for no reason. Some disorders, like narcolepsy (frequently falling asleep against the will) and sleep paralysis (the mind wakes up while the body is still paralyzed), are believed to be connected with an imbalance in the flip-flop switch neurons.

The wake-up nerves

In 2016, a study published in the Nature Neuroscience gave us important information regarding the sleep-wake process. In fact, the scientists discovered a nerve circuit in mice that is responsible for waking up. When stimulated, a group of nerve cells causes cortical arousal – that is, waking up. However, scientists have managed to wake up the animals in this way from NREM sleep and even anesthesia! However, they couldn’t wake them up from REM sleep.

They even managed to get the mice to experience longer NREM sleep and even get into deeper stages of sleep by silencing those nerve cells. The nerve cells they talk about connect the lateral hypothalamus and the ventral thalamus in the brain. GABA nerve cells from the hypothalamus are found to inhibit GABA cells in the thalamic reticular nucleus (TRN). This nerve circuit is what the researchers stimulated and silenced.

GABA is a neurotransmitter whose role is to inhibit other neurotransmitters, helping us relax and fall asleep.

The bicycle model – potassium vs sodium

A chemical-substance aspect was brought into the picture when a study published in 2015 presented some interesting findings. The researchers found that high sodium levels in nerve cells awaken an animal, whereas high potassium makes the animal asleep.

What is even more interesting is that the same process governs the sleep-wake cycle in insects and mammals. Further, the sodium-potassium levels were observed to produce the same results in nocturnal (active at night) and diurnal (active during the day) animals. The scientists call it the bicycle model.

The wake-up genes

Certain genes are tightly connected with our sleep needs and habits. For example, a mutation in the DEC2 gene causes people to sleep shorter, as they have a higher amount of a protein that stimulates arousal. On the other hand, a mutation in CRY1 is connected to a slower, ‘later’ circadian clock compared to those who don’t have it.

However, more genes play a role in our circadian clock. The circadian ‘master genes’ are CLOCK and BMAL1. But they are not alone – they are affected by other genes and their proteins and in a complicated way, they all together ensure our sleep-wake cycle functions properly.

Additional resources

  1. Herrera C. G, Cadavieco M. C, et al. Hypothalamic feedforward inhibition of thalamocortical network controls arousal and consciousness. Nature Neuroscience. 19, pages 290–298 (2016) December 21, 2015. https://www.nature.com/articles/nn.4209 Accessed January 27, 2019.
  2. DiTacchio L, Le H.D, et al. Histone lysine demethylase JARID1a activates CLOCK-BMAL1 and influences the circadian clock. Science. September 30, 2011. https://www.ncbi.nlm.nih.gov/pubmed/21960634 Accessed January 27, 2019.
  3. Flourakis M, Kula-Eversole E, et al. A Conserved Bicycle Model for Circadian Clock Control of Membrane Excitability. Cell. August 13, 2015. https://www.ncbi.nlm.nih.gov/pubmed/26276633 Accessed January 27, 2019.
  4. Hirano A, Hsu P. K, et al. DEC2 modulates orexin expression and regulates sleep. PNAS. March 27, 2018. https://www.pnas.org/content/115/13/3434.short?rss=1 Accessed January 27, 2019.
  5. Patke A, Murphy P. J, et al. Mutation of the Human Circadian Clock Gene CRY1 in Familial Delayed Sleep Phase Disorder. Cell. April 6, 2017. https://www.cell.com/cell/fulltext/S0092-8674%2817%2930346-X Accessed January 27, 2019.

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