Circadian Rhythms

An Independent Project by Monika Nemcova ’19

Part 4 of 4

Circadian Rhythms

This is the final blog post on my series about sleep. Last time, I wrote about the relationship between sleep and learning. Today, I would like to focus on why do we, as mammals, tend to become sleepy at roughly the same time every day. So, what makes us want to go to sleep? And what keeps us awake during the day?

The intricate system in charge of our sleep-and-wake patterns comprises of two so-called drives, homeostatic and circadian. The drives (sets of processes promoting an action) act in opposition [1], balancing each other – in the same way as the two conflicting forces, the gravitational and the centrifugal, balance the Earth on its orbit. However, unlike the forces affecting the Earth, the homeostatic and circadian drives change in size throughout the day – which allows us to transition between sleep and wakefulness.

Homeostatic drive

Homeostatic are any processes that organisms use to maintain stable conditions in their bodies. Homeostatic processes, for example, keep the blood levels of oxygen and sugar stable or maintain the optimal body temperature. Our bodies naturally strive to keep the inner conditions consistent and if an unusual spike in any chemical occurs, there are mechanisms that return said chemical on its normal level [2].

But how does that concern our sleep? Enter adenosine, the neurotransmitter I already wrote about in my second blog post (quick reminder: it makes us sleepy and caffeine functions by blocking it). Adenosine, alongside with other chemicals, builds up in the brain as we are awake – the longer we stay awake the more adenosine there is and, in turn, the sleepier we are. As you can see in Fig. 1, when adenosine levels reach a certain point, we feel sleepy enough to go to bed. During sleep (shown as the purple field), the adenosine levels get flushed out of the brain. That is why it is called the homeostatic drive – when there is too much adenosine, the body employs mechanisms to get rid of the chemical [1].

In addition, adenosine build-up explains how does sleep debt work. In the picture, you can see that after a night full of sleep, the adenosine levels are fairly low. But what happens when we do not allow ourselves enough time in the bed to get rid of all of the adenosine? Well, it just stays in the brain – and as the day progresses, the build-up starts at the levels left there from the previous night, not zero. That is the reason why we feel so horribly tired the day following insufficient sleep or even an all-nighter. Longer time in the bed effectively erases the sleep debt by decreasing the adenosine levels. Nevertheless, if we, once more, do not sleep enough, the morning baseline amount of adenosine increases again. That continues until the body cannot put up with the adenosine levels anymore. Then it just forces us to sleep [1] – and that is all the missed first periods and slept-through films, classed or ASM.

Fig. 1 Homeostatic and Circadian Drives (

Circadian drive

However, if sleep was determined only by the homeostatic drive, the time when we go to sleep and wake up would not matter. Yet very few of us thrive in a regime with a supposed activity peak around 4 a. m. and time for sleep around midday. Why do we naturally tend to sleep during the night and be awake during the day? And how does the brain regulate it?

The answer lies in the second cycle that drives sleep and wakefulness – the circadian rhythm. “Circadian” comes from the Latin words for “around” and “day”, so it won’t come as a big surprise that the circadian rhythm acts as an inner clock for many species, from plants and bacteria to animals. So while the homeostatic drive tells us that we are sleepy when we stayed up for late, the circadian rhythm tells that is is time to go to bed because it is past midnight [3]. The fact that we have inbuilt time makers that go beyond detecting the outward cues (such as the amount of sunlight outside) has been experimentally proven. A group of volunteers was left to live in total darkness for several weeks and their sleep-wake cycle still exhibited periodicity. However, without the outward visual clues, the average length of “one day” (period of wakefulness followed by a period of sleep) was about 25 hours. As a result of that, the volunteers went to sleep about one hour later every day – so after 6 days the difference between the time outside and their inner clock was the same as between the East Coast and Europe [1]. In normal conditions, the human inner clock synchronizes itself daily with environmental clues. This agility marks the second important characteristics of the circadian rhythm: it can adapt to various outward signal. That is what happens when we travel to a country in a different time zone – the inner clock slowly shifts so that the perceived clues match the intrinsic signals. Another peculiar thing our inner clock can do is to change the ratio of “night” and “day” – in the past, people in the Northern Hemisphere slept more during the long winter nights and less in summer. And last but not least, even the length of the circadian period can change. I already talked about the shift from the natural 25 hours period to the 24 hours period we exhibit normally, but, in fact, human beings can be entrained to accept anything between 23 to 25 hours as the length of a “day.” [1] Interestingly, a day on Mars lasts 25 hours [4], so at least our internal clock wouldn’t pose a barrier for possible future colonization of the red planet. I have never realized how important that is – it would be very inconvenient and unhealthy for the first colonists to cycle out of rhythm with the outward cues.

So, returning to the Fig. 1, circadian rhythm prompts our brain to go to sleep roughly around the same time every day. In mammals, the center for keeping track of the circadian rhythms is called the suprachiasmatic nucleus (SCN) [3]. But keeping track of time is not something impressive in the terms of our body – experiments showed that a wide array of cells are able to do that, from the cells of lungs and liver to the ones of skin. What is truly unique about SCN is its position next to the ending of the optical nerves. SCN’s timekeeping system is the only one in the body that can actively respond to visual cues and thus synchronize the inner time with the perceived outward time [3].

In addition, SCN helps to maintain a healthy sleep-wake cycle in other way: by initiating the circadian drive. I started talking about the circadian drive as the opposing force to the homeostatic drive but then went on about the circadian rhythm. It was necessary to understand the periodicity of the process but now I can finally explain how exactly does the circadian drive influence wakefulness. The circadian drive allows us to have a single period of consolidated wakefulness [1]. It is basically a signal from SCN to neurons that release wakefulness-promoting neurotransmitters, such as monoamines or acetylcholine [3]. If we did not have the circadian drive, we would be able to remain awake only for a few hours – after that the homeostatic drive would force us to go to sleep. After short rest, we would wake, be active for a while, and had a need to go to sleep again [1]. One can surely imagine that hunting, foraging or any other complicated activity would be severely hindered by that. So the circadian drive, which acts as the opposing force promoting wakefulness, is very important for the success of human or and many other bigger species. As you can see in Fig. 2, even though the upper arrows symbolizing adenosine levels increase as the day progresses, the wakefulness levels (the blue line) remains constant. That is because the circadian drive (lower arrows) gradually increases as well. In the evening, the circadian drive decreases but the homeostatic drive stays strong – as a result, we become tired and fall asleep. In the morning, the situation is reversed – the adenosine levels have decreased and the circadian drive, timed by the circadian rhythm in SCN, wakes us up [1].

Fig. 2 Intrinsic factors influencing the sleep-wake cycle
Fig. 2 Intrinsic factors influencing the sleep-wake cycle (

I hope that you have found the mechanism of the sleep-wake cycle as fascinating as I have.


[1] Lee, T. (n.d.). Sleep occurs as a circadian rhythm [Video file]. Retrieved from

[2] Rodolfo, K. (2000, January 3). What is homeostasis? Scientific American. Retrieved from

[3] Wright, K. P., Lowry, C. A., & LeBourgeois, M. K. (2012). Circadian and wakefulness-sleep modulation of cognition in humans. Frontiers in Molecular Neuroscience, 5(50).

[4] Mars Facts [Fact sheet]. (n.d.). Retrieved May 8, 2019, from Mars Exploration website:


To Sleep or to Stay up Studying, That Is the Question

An Independent Project by Monika Nemcova ’19
Part 3 of 4

In my Spanish class, one of the girls summarized the universal student’s dilemma: we can either study, have a social life, or sleep – and as our time is not infinite, we manage to do only two of the three options. Well, most of us do not consider eliminating friends and becoming a hermit a viable life option. And at Andover, studying is really not optional – which leaves sleep as the least important activity. Nights thus become an endless reservoir of time which is spent either by writing that English essay or Snapchating with a well-meaning friend. For my whole year at PA, I have never met someone saying that getting a good night of sleep was their priority. Yet, as I try to argue in my series of posts about the importance of sleep, sleeping well is one of the biggest factors that influence our behavior and our performance in life. In this article, I would like to show you that the distinct choice between studying and sleeping does not exist – as the latter directly enables the former. In order to learn, the brain simply requires sleep.

When thinking about the role of sleep in learning, I remembered my dad’s childhood story that has never ceased to fascinate me. Back in the seventies, the Czech Republic still had a communist government, that made Russian a compulsory subject in all schools (as a nod to the USSR, which backed the regime). My dad, never one for learning languages, hated his Russian lessons with a passion. When he was in sixth grade, his Russian teacher insisted on learning long, lyric poetry by heart as a part of the curriculum. No one expected much of my dad. But he surprised everyone by a fluent recitation. He explained to me that he had found out that if he studied the poem straight before going to sleep, he then slept very poorly but dreamt about the poem. In the morning, he could recall it without problems. In fact, as he was telling me the story, he was still able to recite the poem, thirty years after.

The story of my dad might be an extreme case, but the relationship between dreaming about a task and improvement in that activity has been experimentally established [1]. In 2010, researchers taught two groups of people how to navigate a 3D maze. After the learning session, one of the groups went to sleep and the second one remained awake. In the napping group, the subjects who reported dreaming about things associated with the maze fared significantly better in the re-testing of the navigation. In contrast, no such distinction appeared in the awake group – the performance of the subjects was not affected by thinking about the maze. The researchers were careful not to generalize the findings as direct causation between dream experience and memory consolidation. Instead, they proposed that both the dreaming and the improvement of the task were the results of the processes of “memory reactivation and consolidation in sleep” [1]. So dreaming about the task would be just a side product of an efficiently learning brain.

However, that still does not explain how do these “processes” function, nor, for that matter, why was my dad’s learning technique effective only when he studied directly before going to bed. In order to understand that, we need to know a bit about how learning functions. The neurons in our brains are connected in intricate nets and pathways – one neuron always receives inputs from many others and based on the type and strength of the signal it receives, it either fires as well or stays silent. However, this system is not static. Both external (seeing a member of your tribe get eaten by a tiger because he was too loud) and internal (feeling pain after trying to touch fire) stimuli can affect the strength between the individual neurons. So in my first case, the connection between the neural pathway responsible for being stealthy and the pathway recognizing tiger territories strengthens. In the second case, the pathways for “great things to touch” and “fire” become less connected. It is not that easy but that is the basic principle. When the connection between two neurons strengthens, the neuroscientists say that long-term potentiation (LTP) has occurred. Weakening connection is called depotentiation. The last thing we need to know about learning is that the strengthening of the neural connections can be either short-term or long-term. A new experience evokes a short-term change, which, if it were left so, would disappear after four to six hours [2]. The brain needs to further strengthen the connection to make it last. And that is where sleep comes in.

Figure 1. The connections and firing patterns of neurons are vital in learning (Retrieved from

Last remainder: LTP and depotentiation are chemical processes and as such depend on the brain’s own levels of chemicals, called neurotransmitters. I talked about neurotransmitters at length last time, so just a quick review relevant to learning. In REM sleep, the most prominent neurotransmitter is acetylcholine and the levels of other chemicals are low (for our context are important norepinephrine and serotonin). In NREM sleep, acetylcholine is low and both norepinephrine and serotonin occur at moderate to low levels. The neurotransmitters occurring in the brain in different sleep phases determine whatever and how the synapses can be strengthened [2].

REM Sleep

It has been experimentally established that when we learn something new, the proportion of REM in our overall sleep increases. This effect appears only when we actually learn and improve, not just all the time when we try to learn [2]. When we master that task, the amount of REM falls to normal [3]. That alone would be a good indicator that REM sleep somehow contributes to the learning process. However, there is also another proof in favor of that theory – the presence of the before-mentioned neurotransmitter acetylcholine. Acetylcholine makes the synapses (connections between neurons) especially plastic, which allows them to undergo either LTP or depotentiation [2].

LTP occurs when the neuron at the synapse fires in accordance with the general firing pattern of the brain – that EEG diagram pattern which I talked about last time (during REM, the firing pattern looks very much like the pattern of wakefulness). Depotentiation, a process as equally important for learning as LTP, is the result of a neuron firing in-between the pattern seen on the EEG. Also, depotentiation appears only in the absence of both norepinephrine and serotonin – which, again, makes the REM phase of sleep ideal for this process, as the levels of these neurotransmitters are at their lowest during REM [2, 3].

NREM Sleep

We have known for a long time that NREM sleep is also important for memory consolidation – the neurons which fired during the learning process were recorded firing again in the same order, albeit in an accelerated pattern (up to 300x). However, there is one obvious obstacle to proposing that NREM sleep also contributes to LTP – namely the absence of acetylcholine. Without acetylcholine, the short-term LTP potentiation, which happens during REM, cannot be initiated. However, it appears that NREM sleep allows the short-term LTP previously established during the REM phase to be consolidated into the more permanent long-term LTP. In favor of this hypothesis speaks the fact that protein synthesis necessary for long-term LTP notably accelerates during the NREM [2].

In addition, NREM sleep seems to contribute to depotentiation of the unused or even obstructive synapses [2].

Figure 2. Sleeping properly is key in the learning process (Retrieved from

Now we can finally determine the real-life consequences of insufficient sleep. Because the REM phase is the only time when brain has high levels of acetylcholine and simultaneously low levels of other, obstructive neurotransmitters, it is the only time when LTP can be initiated fully. Experiments determined that subjects that were sleep deprived after a learning session showed no performance improvement following day [3]. That is one thing to consider – if we do not get enough REM sleep, learning simply does not occur. Going to sleep might thus be the most effective thing to do before a test, instead of trying to revise the material one more time. Also, subjects allowed to go to sleep immediately after a learning session had especially enhanced performance [3] – which probably explains my childhood mystery concerning my dad’s miraculous technique of poetry memorization. So I hope that the relationship between sleep and learning is less mysterious now (also, do not trust it when someone claims to learn something new while sleeping – it is a myth originating in faulty data analysis during the early twentieth century and as such was debunked in the 50’s [4]). Next time, I would like to focus on circadian rhythms and how do they affect both our sleep and our daily routines.



[1] Wamsley, E. J., Tucker, M., Payne, J. D., Benavides, J., & Stickgold, R. (2010). Dreaming of a Learning Task is Associated with Enhanced Sleep-Dependent Memory Consolidation. Current Biology, 20(9), 850-855.

[2] Poe, G. R., Walsh, C. M., & Bjorness, T. E. (2010). Cognitive Neuroscience of Sleep. Progress in Brain Research, 185, 1-19.

[3] Maquet, P. (2001). The Role of Sleep in Learning and Memory. Science, 294(5544), 1048-1052.

[4] Kang, S. (2018, October 28). Can you learn in your sleep? [Blog post]. Retrieved from Brainy Sundays website:


Neurobiology of Sleep

An Independent Project by Monika Nemcova ’19
Part 2 of 4

My first week of studying the mechanisms behind sleep revolved mainly around how different neurotransmitters create and affect the three basic states of the brain: wakefulness, REM sleep, and NREM sleep. But firstly, we should define what exactly these states mean. Neuroscientists recognize three standard, easy-to-measure characteristics that are used to define the brain states: EEG in the cortex, eye movement, and muscle tone. They are in the picture below. All of them measure electrical activity in certain areas. The first line, EEG, shows the activity of the brain. It is easy to spot the strange similarity between wakefulness and REM sleep in that first line: both have low voltage (seen as shorter marks on the graph) and high-frequency (the marks are close to each other) discharge patterns. It makes sense: dreaming, which happens during REM, often resembles our waking hours, so similar circuits are used to process it [1]. However, there is one interesting exception – our prefrontal cortex, active during wakefulness, is turned-off in the REM phase. The prefrontal cortex is the part of the brain that is responsible for decision making and behavior modulation. So, as it turns off during REM, in dreams we often do things that we would never, ever do awake [2].


REM Chart
Figure 1. Copied from Vazquez et al. J Neurosci 22:5597 – 5605, 2002


The second characteristic used to distinguish between the three brain states are the eye movements, noted as EOG in the picture. Eyes move the most when we are awake (even when we do not change their position conscientiously) and are still during NREM. During REM (which stands for rapid eye movement), they occasionally twitch under eyelids – that could be seen as irregularity on the otherwise flat graph [1].

The third line stands for muscle tone – how much does the body move; the less it moves, the lower the muscle tone. Quite obviously, the biggest is during wakefulness. After that, we are the most active in NREM – that is the phase when we move in the bed. Or, in the case of the less popular individuals for bed-sharing (such as myself), the phase when we steal all the pillows and kick any unfortunate person sleeping nearby. During REM, muscle activity is actively inhibited – probably as a preventive measure so that we could not act on our dreams [1].

While these three characteristics are useful in classifying the state the brain is in, it does not tell us what caused it to be so. As in many other cases in the body, the regulation of the sleep-wake cycle depends upon releasing site-specific chemicals, which, in turn, promote or inhibit the release of other chemicals. In the context of the brain, they are called neurotransmitters. Many neurotransmitters fulfill also other roles than only regulating sleep, so an average student has at least heard the name of many of them – serotonin, norepinephrine (also called noradrenaline), dopamine, acetylcholine, etc. When the electrical signal within a neuron is strong enough, it prompts the release of neurotransmitter – each neuron can do that only with one. So if the neuron releases serotonin, it is called serotonergic; if acetylcholine, cholinergic. The neurotransmitter then acts as a messenger between two neurons – the second neuron can fire more or less rapidly as the result of the chemical. It is important to note that naturally, the neurotransmitters occur only in the small space between two neurons.


Figure 2. How neurotransmitters allow the signal transduction between two neurons. Copied from


That allows them to be site-specific. For example, one neurotransmitter called GABA is normally the chief promoter of NREM sleep. However, if it is released in a specific region of the brainstem called the pontine reticular formation, it inhibits REM and promotes wakefulness. When we take sleep medications (or any other drugs affecting the central neural system), our whole brain suddenly bathes in the neurotransmitters. That can account for some counter-intuitive results of some sleep medication. Most of the sleep drugs as well as the drugs used to induce general anesthesia work by promoting the effects of the beforementioned GABA. It works very well in most of the cases. However, in some patients, the drugs can promote GABA activity in the pontine reticular formation, which eliminates sleep. That is extremely unfortunate especially in children when instead of calming down before an operation, the stressed offspring becomes even more agitated [3].

The chemical cocktail of the brain is complicated but fairly well-understood. Studying sleep has the imminent advantage that it is an all-animal phenomenon, so a lot of studies could be accurately done using animal models. To simplify it, the three categories of brain states correspond with increased levels of certain neurotransmitters. The state of wakefulness is associated with high amounts of released monoamines – a group of chemical compounds where belong also serotonin and norepinephrine. They play a permissive role in sleep occurrence – it basically means that sleep can begin when their levels are low. Some anti-depressants, which work on the basis of increasing serotonin levels, can thus cause insomnia as a side effect [4]. Another important neurotransmitter is called acetylcholine. It occurs in the brain in high concentrations during both wakefulness and REM sleep. In fact, from the chemical point of view, the main difference between the REM sleep and wakefulness is the ratio of monoamines to acetylcholine. When we are awake, their levels are roughly similar. During REM sleep, the monoamines level plummet but the acetylcholine levels stay consistent [1]. I am saying levels – again, do not imagine brain bathing in acetylcholine; the neurotransmitters are released between two neurons and immediately recycled. The fact that the brain uses acetylcholine (and, therefore, the same circuits) in both wakefulness and REM sleep, again provides some rational basis why dreams resemble our waking reality so much.

As for the NREM phase – the traditional, if not a bit boring, sleep in which we spend the majority of our sleeping time, the main neurotransmitter there is the beforementioned GABA. However, I would like to talk mainly about another neurotransmitter associated with NREM sleep, adenosine. Adenosine, as in adenosine triphosphate,  is the breakdown product of the famous energy-storing molecule ATP. It is relevant to us because caffeine acts by blocking the receptors for this sleep-promoting neurotransmitter. As we are awake, increasing amounts of adenosine are released. It effectively determines the length of time we can be alert – as adenosine builds up, we become to feel tired. When we go to sleep, the adenosine levels gradually decrease – the more we sleep, the bigger the decrease. That is the biological basis why we feel more rested and alert after a night full of sleep. Caffeine blocks the adenosine receptors and thus keeps us awake [5, 1]. That is maybe something to think about – caffeine does not make us less tired, it just blocks our ability to recognize how tired we are.

So that is all from me about the neurobiology of learning. Next time, I would like to focus on circadian rhythms and something important for all students: the biological basis of learning and how is that affected by sleep.



[1] Brown, R. E., Basheer, R., McKenna, J. T., Strecker, R. E., & McCarley, R. W. (2012). Control of Sleep and Wakefulness. Physiological Review, 92(3), 1087-1187.

[2] Baghdoyan, H. A. (n.d.). Historical Overview: Brainstem & Forebrain [Video file]. Retrieved from

[3] Baghdoyan, H. A. (n.d.). Wake & REM: GABA [Video file]. Retrieved from

[4] Baghdoyan, H. A. (n.d.). Wake & REM: Monoamines [Video file]. Retrieved from

[5] Baghdoyan, H. A. (n.d.). NREM: Adenosine [Video file]. Retrieved from

Vazque, J., Lydic, R., & Baghdoyan, H. A. (2002). The Nitric Oxide Synthase InhibitorNG-Nitro-l-Arginine Increases Basal Forebrain Acetylcholine Release during Sleep and Wakefulness. Journal of Neuroscience, 22(13), 5597-5605.

Why Do All Animals Need to and How Do They Sleep

An Independent Project by Monika Nemcova ’19
Part 1 of 4

Even though sleep theoretically comprises a third of one’s life, an educated layperson knows basically nothing about it. I personally got through almost twelve years of rigorous formal education without getting to know more than that sleep is healthy (but why is it healthy I couldn’t tell) and that its amount per night should approach the magical number eight. I have, like everyone else at Andover, experimentally determined that if one doesn’t get enough of sleep, the next day feels like personal hell. Somewhere at the corners of my brain hovered information that there are two kinds of sleep – REM (as in “rapid eye movement” – that is when dreaming happens and eyes move rapidly below the eyelids – hence the name) and NREM (“non-rapid eye movement” – the peaceful slumber we don’t remember). This spring, I have decided to end this ignorance of mine and do an IP on sleep to finally understand this elusive phenomenon, which probably influences our day-to-day lives more anybody thought. Because I think that it is important that people know more about sleep, I will post here the weekly summaries of my readings, so everyone could see it.

Even though humanity has slept from its very beginnings, the study of sleep by itself is a very young field. Sleep came to the attention of the scientists in the early twentieth century when Sigmund Freud put forth that dreams contained messages about one’s suppressed desires and that they are crucial in unlocking one’s unconsciousness. While his claim is now generally regarded as pseudoscience (because it is impossible to prove or disprove it), it foreshadowed the efforts of future scientists to understand sleep. The breakthrough came in 1950 when a British physicist Robert Lawson during a long train ride noticed that the eyes of sleeping people were twitching under their eyelids [1]. He then spent the rest of the ride observing the sleeping passengers and the frequency of the rapid eye movements. Later, he wrote about this unorthodox experiment in a short letter to Nature [2]. A researcher at the University of Chicago, Nathaniel Kleitman and his graduate student Eugene Aserinsky decided to verify and quantify Lawson’s observations. In 1953, they proposed a relationship between the rapid eye motility observed during the sleep and dreaming, setting thus the now widely-known distinction between REM and NREM sleep. When they awoke sleeping people in the middle of their REM cycle, the vast majority of them was able to recall the dream they had or at least knew they were dreaming. In contrast, when they awoke subjects in the NREM phase, the overwhelming majority of the people could not remember their dream. Kleitman and Aserinsky also measured the interval between the individual REM phases and concluded that “An eye movement period first appears about 3 hr after going to sleep, recurs 2 hr later, and then emerges at somewhat closer intervals a third or fourth time shortly prior to awakening.” [3] When our sleeping cycle ends with the REM phase, we are able to recall the last dream. Their research also showed one of the reasons why it is so important to have a night of uninterrupted long sleep, as opposed to a few hours at night and a handful of naps – the REM phase starts only after several hours of sleep. The REM phase is crucial for learning and memory consolidation (I will discuss why is it so at some later point) [4].


Figure 1. Copied from


However, even after more than half a century of study, some aspects of sleep remain a mystery. For example, no one is sure why sleep evolved in the first place. Sleep seems like an evolutionary disadvantage – a period of time when an individual is vulnerable to the attacks of predators and cannot look for food or potential mates. Yet all animals sleep one way or another and mammals have the same sleep patterns as we do, complete with the REM and NREM phases. There must be a definitive evolutionary advantage of sleeping.


Figure 2. Copied from


Some propose that animals have evolved to eliminate the time spent by running around and being vulnerable to predators. Asleep, they are hidden, quiet and thus better protected. However, the counterargument presents itself very readily here – the individuals are less likely to escape the predators while asleep. Another theory proposes that sleep evolved to conserve energy – while we sleep, our metabolism, body temperature, and caloric demand all decrease [1]. That is, by the way, the reason why we do not even notice that we regularly do not eat up to ten hours because of sleep. If we don’t go to sleep, the body demand energy as usual – everyone has probably experienced gnawing hunger around two in the morning while desperately trying to finish an essay. Sleep also might have evolved as a time when the body could repair itself [1]. Personally, I have noticed that when I don’t sleep enough, my skin roughens, I’m more prone to acne, and I get sick easily. An important topic for students is also the role of sleep for memory consolidation [1]. We probably cannot determine a single reason why sleeping evolved but we can be sure that now it serves several different important functions and when we do not get enough of it, the body suffers greatly. Next week, I will focus on the neurobiology of sleep.



[1] Mar’i, J. (n.d.). Experiment: Sleep. Retrieved March 25, 2019, from

[2] Lawson, R. (1950). Blinking and Sleep. Nature, 165, 81-82. Retrieved from

[3]   Aserinsky, E., & Kleitman, N. (1953). Regularly Occurring Periods of Eye Motility, and Concomitant Phenomena, During Sleep. Science, 118(3062), 273-274.

[4] What is REM Sleep? (2016, December 1). Retrieved March 25, 2019, from

The A-MAZE-ing Chicks…

Take On The Labyrinths of Room 103!


After a successful relay race last Monday— though some chicks were a tad distractible— Animal Behavior students have spent the past week studying associative learning and spatial cognition. This was achieved through two experiments: teaching our chicks to turn in a circle on command, and determining their learning abilities in the context of navigating a simple Y-maze.

Pictured below is Jan’s chick, Colonel Sanders, who was the only triumphant twirler in our class.

For the second experiment, my group constructed a Y-maze out of shoeboxes wherein one path from the fork would lead to food and freedom, and the other to a dead end. We tested the accuracy of Ferdi, Colonel Sanders, and a third chick over the course of five runs.

Our data depicted a significant decrease in time taken from Run 1 to Run 2 immediately followed by an outlier increase for all three birds in Run 3. Then, as the timing decreased for all birds aside from Ferdinand (who got distracted) in Runs 4 and 5 respectively, the data appeared to indicate that chicks can retain their learning of a Y-maze for a short amount of time, needing to “re-learn” the route before gaining any form of proficiency.


Can’t Help Falling In Love With…

The Return of Animal Behavior!

Guest Post By EMMA BROWN ’19

Welcome to Animal Behavior 2018! After the eventful happenings of last Thursday evening, the arrival of baby chicks to dorms and homes was a much-appreciated change of scene. Below is a picture of my chick, Franz Ferdinand, who has a certain fondness for cuddling and attempting to roost in my hair. (Currently, as I type, Ferdi is making his best efforts to turn my attention away from my laptop by means of walking all over the keys.)

This weekend has been devoted to getting our chicks prepared for an obstacle course on Monday. This will test the strength of the filial imprinting process for each chick. At this age, chicks imprint almost immediately. After all, they’re just barely a few days old! As to provide a protective figure for them, it is important to bond with your chick early on. I have been doing this by feeding, cuddling, talking and singing to, and spending as much time with Ferdi as possible. Additionally, as chicks are attracted to the color red, I’ve been wearing solely red shirts for the past few days in true, traitorous Exonian form. (Love knows no bounds.)

Come back next week to see how my Elvis-ballad-loving chick performed for his debut race!

Schooled by the Fish

Animal Behavior Learns about Schooling of Fish

Guest Post by Carley Kukk ’19

This week in Animal behavior we researched the tendency of fish to school. Certain fish school, such as Silver Tail Rasboras, in order to protect themselves against predators. They truly embrace the idea of strength in numbers. In contrast, other fish, like red wag platys, do not school because their slow-moving bodies would not benefit from swimming in groups if a predator came along.

For our lab, Dr. Bailey asked us to come up with a procedure that could identify schooling in fish. My group and I decided to insert a piece of plastic with a hole into a tank with two different amounts of fish on each side. We would time how long it takes for all of the fish to reunite (or swim through the hole and form a school). Our fish, the red wag platys, are non-schoolers, so they didn’t mind the separation from their peers or didn’t reunite.

After we completed our own procedure, Dr. Bailey gave us her own version to test. We drew lines on the outside of the glass fish tank indicating sections 1-4. We separated all of the fish except one into a separate bowl next the side of the tank with a barrier so they couldn’t see the lone fish. After 3 minutes of allowing the lone fish to relax after his separation, we removed the barrier and tracked which section the lone fish remained in. If he was in section 1, closest to the other fish, for the entire 10 minutes, schooling occurred. Yet the red wag platys distributed themselves evenly across the sections, indicating no sign of schooling.

Ultimately, Dr. Bailey’s procedure was more effective in determining whether schooling occurred, yet the lab was extremely interesting and the fish, especially the red wag platys, were/are super cute!

Squirrels and Crayfish!

Animal Behavior Learns About Foraging and Territoriality

Guest Post by Carley Kukk ’19

The last two weeks of animal behavior have been pretty busy with learning about foraging behaviors and territoriality. To explore foraging behaviors, we utilized an abundant resource on campus: squirrels!


We set up a station next to multiple trees around campus with 4 piles of peanuts. Two piles were 2m from the tree while the others were 6m. One pile at a certain distance had unshelled peanuts and the other shelled. During our double block, we observed squirrel activity. Although we weren’t so lucky in sighting any squirrels (weird, right?), we learned the typical trend for this activity. Unshelled peanuts closer to the tree are a more popular choice because unshelled peanuts require less handling time (aka: less energy) and they are closer to a tree where a squirrel is safe from predators.

In another experiment performed this previous week, we tested the theory that residents are more likely to dominate intruders in a battle over territory. We placed a crayfish (who is extremely territorial) in a tank overnight to establish it’s dominance over the territory.


The next morning we added an intruder crayfish: one larger and one of the same size. The resident crayfish usually dominated an intruder of the same size, yet was defeated by an intruder of a larger size.


Like a Chick in a Maze

Animal Behavior Continues Working with Chicks

Guest Post by Carley Kukk ’19

During our last week with the chicks, we focused on teaching them how to get through a maze using associative learning. We constructed a simple Y maze with leftover shoeboxes and placed a small pile of food at the end.


The food acted as a positive reinforcement if the chicks successfully completed the maze. Hopefully, they would later associate the correct end of the maze with the food.

In our experiment, we used 2 chicks to strengthen our data. Each chick surprisingly ran their fastest time through the maze on their first try. This was probably a fluke as later proved in the data where the chicks always explored the other end of the maze before completing it.

Eventually it took around 30 seconds each to complete the maze. There were in total around 7 trials for each chick. They finally began to associate the ending with food and ultimately learned through operate conditioning the correct way to complete our y-maze.

Chirping on the Great Lawn

Dr. Bailey’s Animal Behavior Class Brings Joy to Campus with Baby Chicks!

Guest Post by Carley Kukk ’19

Last week in my Animal Behavior class, we set out to imprint newly-born chicks. The chicks spent 2 nights with each student whether that be in our dorms or houses. Since chicks are attracted to movement and the color red, we tied a red bandana around our ankles once the chicks were adjusted to the sound of our voices. I tried to spend as much time as I could with my chick, Carter, so I held him while doing homework or in any possible moment.


Chicks can imprint on something else after 4 hours, so it is crucial during the initial 32 hours to spend time working with them. I set up an obstacle course around my dorm room and had him jump over pillows and pens while following me. The harder the obstacle course, the stronger imprint because the chick will be focusing on you more. It was hard not to accidentally step on him! You would be surprised how fast their tiny legs can move.

At the end of the two days, Dr. Bailey held a class-wide relay race to determine the chick with the strongest imprint. My chick may have won with a time of 11 seconds… (humble brag).

Ultimately over the course of the 2 days, I was able to learn first hand about filial imprinting. I even made a new friend… 🙂