Evolutionary Biology: Sleep Patterns in Mammals

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Table of Contents

Introduction
The Concept of Sleep
Brief Background
Hypothesis one
Hypothesis Two
Hypothesis three
Hypothesis Four
Hypothesis Five
Discussion
Bibliography

Introduction

What selective pressures drive sleep patterns in mammals? Perhaps the most interesting trait that all mammals share is the process known as sleep. Sleep is an essential condition that occurs in mammals and is defined as a naturally recurring state characterized by reduced consciousness and repressed voluntary muscle control. Despite its fundamental role in human and animal life, sleep is, even after decades of scientific research, still quite a mystery in the field of evolutionary science. Why do mammals cease to acquire food and reproduce to subject themselves to such a vulnerable state? This synthesis addresses the question of the origin of sleep in mammals and traces this phenomenon by studying the evolution of the mammalian brain and suggesting possible external factors that affect sleep patterns.

The Concept of Sleep

Before embarking on the considerations of selective pressures that drive sleep patterns, it is important to briefly clarify the concept of sleep. Sleep is induced by the connection of the sleep-active neurons that are located on the opposite sides of the brain. When this additional inhibitory connection is modeled, uni-hemispheric sleep is generated. “Neuro-modulation of these connections is what makes a possible transition between bi-hemispheric and uni-hemispheric sleep respectively” (Rattenborg et al. 2009: 262).

This means that the physiological mechanisms, which are responsible for mammalian sleep, are similar apart from the modifications that have resulted due to evolution. These modifications are responsible for the varying sleep patterns in mammals (Staunton 2005). Most of the experiments undertaken have uncovered the neurological structures that are associated with mammalian sleep patterns. The explanation behind this is that the circadian and homeostatic mechanism is responsible for the sleeping behavior of animals since it alters the sleep-wake switch of mammals thus determining their sleep patterns although it is not well established whether the system is ubiquitous to all species of mammals (Lima et al. 2005).

In mammals, sleep consists of two main states; fast wave-phase sleep (FWS) and Short wave-phase sleep (SWS). They are indicated as “wave phases” because sleep activity is measured by using Electroencephalography (EEG), which records electrical activity along the scalp produced by the firing of neurons within the brain. During FWS, mammals experience frequent periods of rapid eye movement (REM) and are characterized by an elevation in bodily processes.

These REM features include; deep muscle relaxation, sudden eye movements, muscular twitches, increased heart rate, and incapacity to regulate body temperature (Akaarir et al. 2000). In REM metabolism and sensory thresholds also increase to near a point of wakefulness. On the other hand, in SWS mammals experience non-rapid eye movement (NREM), which is a period of slow bodily processes. NREM is the most abundant phase mammals experience during sleep and consists of opposite features of REM. (ie; little or no body movement, slow heart rate). These phases alternate continuously throughout the sleep cycle with NREM being more extensive and are maintained throughout the entire episode.

Brief Background

Historically, it is speculated that poikilotherm vertebrates such as reptiles possess sleep features that serve as the basis for functional sleep patterns in mammals (Aristakesyan 2009). Poikilotherms are organisms that have no self-regulation of body temperature. In poikilotherms, the brain consists of two main structures known as the telencephalon(cerebrum) and mesencephalon (midbrain). Neurologically, the mesencephalon stimulates the telencephalon and promotes wakefulness. These structures are found in most poikilotherms today and elicit a low sleep state consisting of REM, meaning the telencephalon experiences more frequent neural stimulation. So in correlation; the descendants of mammals (poikilotherms) elicit sleep states whereby the “wake” cycle is constantly being stimulated.

This is due to the lack of temperature regulation. Progressively, as mammalian sleep patterns diverged from reptiles, the mesencephalon evolved into a diencephalon, which consisted of the forebrain, midbrain, and hindbrain. According to Aristakesyan:

In the process of evolution, owing to progressing the development of the vertebrate brain, the functional activity is changed both in the structures generating and regulating sleep and in the sleeping structures, i.e., on one hand, there are developed the structures that need sleep and are based on telencephalon, but, on the other hand, there are developed structures of diencephalon, mesencephalon, and rhombencephalon that provide regulation of SWS and FWS. (598)

This piecewise evolution of the mammalian brain resulted in two main waking types; diurnal and nocturnal. During the diurnal activity, the sensory-motor cortex is constantly under stimulation by the midbrain. During the nocturnal activity, this neural stimulation is inhibited by stimulation from the diencephalon. In essence, sleep can be thought of as the process whereby the diencephalon inhibits the activity of the mesencephalon. It is the balance of activity between these two components that produces sleep and regulates REM and NREM patterns. This neurological structure plays an essential part in the evolutionary development of mammalian sleep patterns.

Hypothesis one

Selective pressures exerted by infectious parasites induce mammalian sleep patterns.

Not only do mammals respond to threats of the external environment, but they must also defend against infectious parasites constantly entering the body. Therefore, this hypothesis speculates that sleep evolved to maintain the health of the internal systemic environment that comprises all mammals.

Studies performed by Barton and others show the adaptive patterns of sleep that evolved in response to parasite infection. Barton et al. hypothesize that sleep fuels the immune system and mammals that sleep more should show increased resistance to pathogens. In the study performed, scientists extracted a variety of sleep periods from a variety of mammals. The various species under study consisted of sheep, guinea pig, chimpanzee, mongoose, platypus, and hedgehog.

Using the average times, Barton’s team took immune cell counts for each animal and found a correlation. Results showed that there is a direct relationship between the length of mammalian sleep and the concentration of immunity cells. Specific immune cell concentration can be related to specific pathogen concentration that is being contested; so increased immune cells indicate a higher concentration of pathogen. Ultimately, the study found that mammals with longer average sleep periods have higher white blood cell counts than mammals with shorter sleep periods (Barton et al. 2009). Additionally, it was also found that mammals with longer sleep cycles are infected with fewer pathogens.

A second study performed by Opp (2009) shows a similar trend through the use of cytokines; the chemical signals that coordinate immune response. In the study, researchers have found that with increased antigen concentration, comes increased cytokine release to activate immune cells. According to Opp, “Cytokines directly alter properties of neurons in the mammalian brain including those in regions involved in the regulation of sleep” (Opp 2009: 49).

Further evidence that supports this hypothesis includes a study performed by Beizaeipour and others. This study consisted of triggering sleep response in Drosophila flies through stimulation of the immune response. Although Drosophilae are not mammal, genetically they are very similar and the results from this experiment are analogous to mammalian studies. “The observation that the immune response promotes sleep in Drosophila demonstrates an additional feature of insect sleep that is shared with that in mammals” (Beizaeipour et al 2010: 119).

In this study, scientists inoculated flies with gram-negative Escherichia coli and monitored how the immune response to infection affected sleeping patterns. Sleep state was indicated by zero activity in the flies. According to results, Drosophila was found to enter a sleep state within one hour following bacterial inoculation. Control flies with little or no infection spent an average of twenty minutes in a sleep state. On the other hand, infected flies showed sleep states averaging to ninety minutes. These results are rather astounding considering the short lifespan of Drosophila.

These findings support the conclusion that sleep enhances immune defense. Because animals subject themselves to this dormant low energy state, the mammals channel resources internally and “adapt” to the selective pressures exerted by pathogens infecting bodily systems. It is possible that antigenic challenge from pathogens selects for increased white blood cell counts, which ultimately selects for increased sleep length.

Therefore, mammals with longer sleep patterns are species whose ancestral lineage was exposed to greater pathogens. Figure 2 illustrates the findings of Barton and others, which shows the direct correlation between white blood cell count and length of sleep in the studied mammals. Additionally, figure 3 shows the correlation between bacterial infection and Drosophila sleep period. As you can see, pathogens play a significant part in mammalian sleep patterns.

Hypothesis Two

Energetic constraints drive sleep patterns in mammals.

The key to the survival and reproduction of all mammals is the ability to acquire energy. If mammals cannot acquire energy to carry out their physiological processes, then lack of energy access can be viewed as a selective pressure. The inability to acquire food in a particular environment selects for sleep expression as a method of energy conservation.

Studies performed by Nelson and others reveal that energy constraints play an essential part in mammalian sleep patterns. In their experiment, researchers monitored the sleep cycle of three bears over the course of three years. During the winter seasons when very minimal amounts of nutrients was available, they found that bears entered a deep state of sleep known as hibernation where very minimal amounts of energy was expended to keep the bear alive. According to the study, at the end of the ninety-seven day winter sleep, the bears had not urinated or defecated, and had lost 25% of their body mass. However, at the end of winter sleep the bears were almost in perfect water balance with normal concentrations of plasma and red blood cells (Nelson et al.1973).

Additional studies performed in 2008 by Capellini and others further support this hypothesis. In the study carried out, researchers extracted data from various scientific articles regarding the sleep traits of fifty-six terrestrial mammals. The information gathered in their analysis includes; sleep period, sleep distribution, body mass, predation risk, and length of REM and NREM sleep states. By comparing these components, the researchers were able to determine whether predation risk or energetic conservation had the greatest impact in driving mammalian sleep patterns. According to the results, there is an association between larger body mass and increased sleep periods.

Therefore, it can be concluded that with a larger body mass, comes more energy expended by the mammal, which elicits longer sleep periods for energy conservation. The study also found that small terrestrial mammals experience to sleep in short frequent patterns due to the need to acquire nutrients more regularly than larger mammals. As stated by the article, “The correlation with size may reflect energetic constraints: small animals need to feed more frequently, preventing them from consolidating sleep into a single bout” (Capellini et al. 2010: 847). Further evidence from the study that reflects the significance of energetic constraints includes the additional finding that even with increased vulnerability to predation; there is still a positive correlation between body mass and sleep period. Figure 4 illustrates the findings of perfectly.

A final study performed by Pravosudov and the company further illustrates the importance of sleep and energy attainment. In this study, scientists view the important role of how sleep promotes memory retention, which is essential to the process of acquiring nutrients. Specifically, it is shown that food-catching animals engage in a system of sleep for two reasons: to promote memory retention and to conserve energy (Pravosudov et al. 2010).

According to the study, “Sleep loss impairs alertness, interferes with the consolidation of recently acquired information and may impair an animal’s ability to acquire new information; therefore, sleep, like foraging, reproduction and predator avoidance, is very likely a necessary component of fitness” (Pravosudov et al. 2010: 533). Energy is a strong force driving patterns of sleep.

Hypothesis three

Mammalian sleep patterns are driven by genetic regulation.

According to Cirelli (2009) who is the proponent this hypothesis; he supposes that there are mammalian genes whose presence in mammals’ genetic makeup induces sleep by prolonging general sleep patterns while others reduce the sleeping periods considerably. One example is the ion exchange channels. In ion exchange channels, two genes have been identified in mammals such as rats and mice; and these genes have been found to regulate sleep patterns through mutagenesis.

These two genes are shaker and sleepless. In the experiment done, mice that were regulated with the shaker gene reduced their sleep patterns from the normal nine hours to three hours per day. Under sleepless gene expression, the mice exhibited similar change in sleep patterns from the normal nine hours to three hours in a day. This shows that the genetic makeup of mammals has an influence on expression of mammalian sleep patterns, which supports this second hypothesis (Cirelli 2009).

In Circadian regulation, there is an interaction of the circadian genes and this determines the circadian rhythmicity. There have been several experiments to test the effect of these genes on sleep. In mice, the two circadian genes namely cryptochrome 1 and cryptochrome 2 were shown to have an impact on the sleep patterns. According to Cirelli (2009) these two genes are associated with higher non-rapid eye movement sleep, which makes mice to sleep more and in the event increasing their sleeping periods. Cirelli (2009) still indicates that there are other genes such as ARNT – like protein 1, prokineticin 2, and neuronal PAS domain protein 2, which are responsible for the different sleep patterns in mammals and are specifically responsible for causing longer sleep patterns in these animals (Cirelli 2009). These corroborating experimental results and conclusions are a clear indication that genes play a central role in influencing sleeping patterns of mammals to different degrees.

Hypothesis Four

Chemical “Pressures” Regulate Patterning of Sleep in Mammals

The regulations of chemicals influence the neural framework behind sympathetic and parasympathetic nervous system function. In my prediction, mammals in environments selecting for large sleeping patterns will show more leniency towards parasympathetic genetic expression suggesting that chemicals induce patterns of sleep. Studies on neurophysiology show that there are various chemical mechanisms that are responsible for regulating mammalian sleep.

A good example of this is the way monoaminergic brain stem nuclei operate. These (monoaminergic brain stem nuclei) are nerve fibers or cells that use monoamine neurotransmitters to transmit nerve impulses. When they are active, they project to the cerebrum of the brain excretions that cause the animal to awaken. In the same way, inhibitory connections between ventrolateral preoptic and monoaminergic nuclei which happens in the sleep active areas of the hypothalamus usually leads to self-inhibition which is by reinforcing self activity (Toth 2003). This inhibiting effect is one that makes up the sleep-wake switch.

In wake, monoaminergic brain stem nuclei are active and the ventrolateral preoptic sleep active area of the hypothalamus (which is the area of the hypothalamus responsible for sleeping tendency) is suppressed while in sleep; and the ventrolateral preoptic sleep active area of the hypothalamus is active while the monoaminergic brain stem nuclei are suppressed when awake. It is the balance of these two chemicals that is responsible for the state transition from wake to sleep or from sleep to wake such that “during the wake period, the homeostatic drive increases due to accumulation of the somnogen following sleep deprivation” (Toth and Verhulst 2003: 229).

Accumulation of somnogen leads to rebounding of sleep thus driving the mammal into a sleep period. Sleep only sets in after the somnogens have accumulated enough to overpower the sleep-wake switch thus switching it from the wake side to the sleep side.

However, when the sleep period sets in, the production of the somnogen reduces and its clearance overpowers its production and this finally decreases the homeostatic drive thus switching the sleep-wake switch from sleep side to the wake side again. This alternation of the somnogen is one that makes up for the sleep and wake period through its regulation. According to the research findings, the physiological pathways that are associated with somnogen are yet to be discovered but some of the factors associated with these pathways have been found and these include metabolic chemical reaction product of adenosine tri phosphate hydrolysis known as adenosine and immunomodulatory cytokines (Baracchi and Opp 2009).

Despite the fact that these chemical reactions induce sleep and wake periods, there is not enough evidence as to whether they have an effect of the expression of sleep patterns in mammals in terms of duration, quantity and quality of sleep.

Hypothesis Five

Predation selects for shorter sleep periods in mammals.

Predation is a strong selective agent when it comes to the sleep activity of mammals. If a particular mammal is found in an environment where predators are abundant, then this setting should select for individuals in the population with the shortest sleep period because they would be the least vulnerable. Therefore, it can be speculated that increased levels of predation in the environment selects for mammals with shorter sleep period.

It is Sanford and others’ contention that mammals in vulnerable settings experience less intense sleep states. In a shock therapy experiment, mice were subject to constant electrical stimulation over a period of time. Although electrical shock is not the same as predation, the stimulating significance is very similar. Results found that mice subject to higher frequencies of stimulation spent significantly less time in NREM sleep states.

The functional impact of these findings was not studied, but it is apparent that the mice experienced more shallow forms of sleep when subject to predatory like stimulation. Instead of experiencing deep unconscious state of NREM sleep, the mice are found in a state of drowsiness. This has been considered a cautious for of sleep to allow mammals some form of predator alertness (Noser et al. 2003).

Other studies have shown that this state of “cautiousness” is dependent on group size and organization. For instance, in large group sizes mammals demographically found on the edge are expected to sleep in a more alert state. It was Alados (1985) who found that individuals living near the periphery of populations experiencing an “edge effect” whereby marginal groups are more vigilant than those at the center.

Discussion

Five hypotheses have been developed in attempt to explain selective forces that drive sleep patterns. First, it was proposed that levels of pathogen infection determine the length of sleep cycles. Hypothesis 2 considers correlation between energy utilization and the benefits of sleep. Thirdly, it was seen that genetic regulation is critical sleep expression. Fourth, sleep expression was viewed from a chemical perspective. Finally, it was determined that predation also contributes to mammalian sleep patterns.

Although each hypothesis can be viewed as feasible in selecting for sleep patterns in mammals, hypothesis two is the most significant. As the hypothesis postulates, energetic constraints influence expression of patterns of sleep in a way that the more energy the animal spends, the higher the sleep duration to lower the metabolic rate and conserve energy. This is the most relevant hypothesis that strongly supports the main thesis statement since it is also backed by concrete evidence from authorities that have done extensive studies regarding evolution of sleep. Based on research findings, it is clear that energetic constraints shape the foundation of mammalian sleep.

The physiological control of sleep in both humans and nonhuman mammals is influenced by the consequences of the waking experience (Langford and Cokram 2010). This means that sleep can be used as a valuable tool in assessment of the welfare of mammals. Mammals exposed to stressful activities, painful events and fatigue, experienced prolonged periods of sleep afterwards than animals exposed to less energy consuming events. Therefore, during the activity, animals spend a lot of energy until they become exhausted and since there is no more energy to spend, the animals are triggered to sleep to reduce the metabolic activity (Chaput et al. 2007).

Since most of the research done have only based on a few species of mammals, I recommend that future researchers should cover a wide variety of mammals so that the conclusions made on the selective pressures that influence mammalian sleep patterns could be made with outstanding evidence and little assumptions. Based on the research done, there is a knowledge gap between circadian sleep based rhythms and sleep based on environmental seasonality that need to be examined. More research needs to be done on ecological factors that affect sleep to add more weight to the energetic constraints affecting sleep.

The connection between the intensity of sleep, natural selection and the physiological needs of mammals must also be focused (Lesku et al. 2008). I also recommend that the area of sleep variation especially in human beings be given attention. No efforts have been put in place to study the reasons behind varying sleep patterns across mammalian cultures (Lesku et al. 2006). This applies mostly to human cultures. It might be possible that ecological conditions are the ones responsible for the varying sleep patterns in various human cultures since it has always been evident that the sleep patterns of city dwellers and those perceived as hunter-gatherers are always different (Kelmanson and Adulas 2002).

When doing research on sleep patterns, I also recommend that the researchers should focus on different environmental conditions of wild and domestic species of mammals. Maybe wild animals express different sleep patterns from the domestic ones due to lack of good shelter, stress and food among other stressful conditions. All these should be examined in details.

Bibliography

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