Why do we sleep?

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         Sleep is a vital component to the life of all complex living organisms. Research in sleep studies have focused on the synaptic connections in the brain and its strength relating to the sleep-wake cycle. One hypothesis is that sleep weakens synaptic connections as a method of winding down after being active all day. Alternatively, sleep has been proposed to strengthen synaptic connections as a method of memory preservation. My focus is on research correlating to weak synaptic connections and its energy renewal process associated with sleep. Drosophila Melanogastor is the focal point as researchers use these fruit flies to corroborate the downscaling hypothesis. The first study demonstrates an increase in significant proteins associated with the synapse when flies were sleep deprived. Continually, these results showed a decrease in the number of activated synapses when proper sleep was achieved. Moreover, further independent research observed gene manipulation within the circadian clock affects the flies synapse, leading to an overall decrease during sleeping. Lastly, NMDAR a molecule associated with memory formation is counteracted in the sleep cycle by slow wave formation and discredits research supporting the strong synaptic connection hypothesis.


As humans, we spend one-third of our lives sleeping to ensure a healthy, normal functioning body. As an important quality to our lifestyle, sleep affects how we feel and perform daily activities and rejuvenates our mind for the next day. Sleep, an unconscious state, allows our brain to be active to complete phases like muscle repair, memory consolidation, and the release of hormones that regulate growth and appetite. As a dynamic process, sleep follows a structure of alternating REM (rapid eye movement) and NREM (non-rapid eye movement) cycles throughout a typical nights rest. During a regular sleep-wake cycle activity generated in the brain controls whether a person is awake or asleep. Neurotransmitters, chemicals involved in nerve signaling, are released from a chemical stimulus and act on nerve cells in different parts of the brain. In turn, sleep is induced when these nerve cells inhibit parts of the brain that function only in the awake stage of the cycle (emedicinehealth, 2010). However, there is an air of mystery surrounding the strength of these synaptic connections during periods of wakefulness and sleep. Nevertheless, sleep research has led me to believe that weaker synaptic connections decrease during sleep to revitalize the brain for the next day's neural activity.

Weak Synaptic Connections

Although research has advanced our knowledge of the processes that are involved in sleeping, scientists are still debating the question of why we sleep. One hypothesis (Miller, 2009) suggests that sleep weakens synaptic connections as a method of winding down after being active all day. The theory operates off the idea that the body sleeps to conserve energy and consolidate space needed for the brain to encode memory the next day. Another sleep hypothesis contradicts the first one suggesting that sleep actually strengthens synaptic connections as a way of preserving our memories. However, two studies with fruit flies have shown the most convincing results of weaker synaptic connections since the beginning of sleep studies. Jeffery Shaw, a graduate student at Washington University, used fruit flies to monitor activities during the day and how this affects their sleep. Shaw's lab manipulated genes in the circadian clock and discovered they could prevent the flies from sleeping properly after a socially active day. The most intriguing evidence came as the fly was only restored in 16 ventral (front) - lateral (side) neurons out of 200,000 neurons in the fly brain and resumed normal sleep patterns. In addition, while monitoring the social activities that induce sleep, Shaw found an increase in the number of synapses between the neurons and the brainstem. While sleeping, the same fruit flies showed a decrease in the synapses giving evidence toward the downscaling hypothesis of weaker synaptic connections (Miller, 2009). The study concluded that the activities during the day controlled the amount of sleep the fruit fly was compelled to take, regulated by the circadian clock. Lastly, the genes in the regulatory process of the circadian clock are also involved in alerting the fly for its need to sleep. Chirelli and colleagues (2009), studied the need for sleep and neuronal plasticity, the ability of neuronal networks to adapt or change, using sleep deprivation. Using Drosophila melanogastor, Chirelli and her team achieved sleep deprivation by shaking vials or forcing males to cohabitate. To effectively test the synapses, Bruchpilot (BRP), an essential component of all excitatory synapses, was measured because of its association with strong synapses in the brain. As sleep was deprived for 6,12, and 24 hours higher BRP levels were discovered compared to Drosophila with normal sleep patterns. In addition, Discs-large (DLG) a post-synaptic protein found at the neuromuscular junction in the CNS was monitored. The results illustrated an increase in number and size of the presynaptic active zones among the sleep deprived test subjects. This pattern continued as they again retested flies that slept at random hours, confirming that proteins increase during sleep deprivation and was not regulated by the circadian clock. In addition, the volumes of major structures in the fly brain were measured during the studies to monitor any change. Since memory and learning is associated with various components of the brain, scientists hypothesize that activity may lead to an increase in volume throughout the structure. The results mirrored the hypothesis in showing an increase in the number of volume of synaptic connections (Chirelli, Gilestro, & Tononi, 2009). Chirelli concluded that their study proved a decline in proteins and the various functions associated with them were dependent upon the need to sleep. The results confirm that the proteins fluctuate on the sleep-wake cycle, not time of day. Lastly, sleep aids synapses in repolarizing to its baseline level to maintain cellular homeostasis. Jan Born, a neuroscientist at the University of Lubeck, says "Together, these findings very clearly demonstrate that one major function of sleep is to reduce, on a structural level, synaptic connectivity in the brain." (Miller, 2009).

Problems with Strong Synaptic Connections

Marcos Frank, University of Pennsylvania School of Medicine, researches the opposing hypothesis of the brain strengthening its connections during sleep. Frank and his team of researchers used a model of the neuronal network to rearrange the neural connections that respond to real life events. They believe that memory formation is the actual making and breaking of these connections during sleep. To test the hypothesis, Frank and his researchers stimulated young, developing animals visually through one eye, covering the other with an eye patch. Immediately following, some animals stimulated were allowed to sleep while others were kept awake and compared to control animals. The control animal used was an animal that was stimulated with both eyes, unlike the test subjects with only one eye. To their amazement, they found a molecule called N-methyl D-aspartate receptor (NMDAR), which was only stimulated once the animal was fully asleep. The molecule is an essential component to the synapse by receiving signals in the form of glutamate and regulating the flow of calcium. The process is started during its wake cycle as it receives the visual input for consolidation. During sleep, NMDAR receives the signal glutamate binds to the receptor opening the ion channel allowing calcium into the cell to turn enzymes on and off. As a result, the synapse strengthens leaving the visual cortex to reorganize its structure. Frank and his colleagues, concluded that during sleep the brain strengthens its connections to process the memory from the days activities. They found that the inhibition of the NMDAR enzyme prevented the brain from reorganizing itself in a normal way. However, the study did not recall memory retrieval but is believed to be the underlying mechanism for the formation of memory (University of Pennsylvania School of Medicine, 2009). Matthew Walker, a psychologist at UC Berkeley, studies sleep deprivation in test subjects in terms of memory. In his sleep study, he took 39 young adults and performed a rigorous memory task that both groups could repeat later. After one group took a 90 minute nap, he made them perform a different task at which they were proficient at learning. Comparably, the group who was up all day had trouble with their capacity to learn. The studies reinforced the hypothesis that our brain uses sleep as a method of consolidating the memory we form visual while we are awake. According to their findings, the longer the brain spends without sleep our minds become sluggish and we slowly begin to lose our ability to function tasks perfectly. Their research has helped conclude that while we sleep our short-term memory storage empties and our brain consolidates making room for new information. Walker and his researchers established that while we are awake our memory is temporarily stored in the hippocampus and then sent to the brain's pre-frontal cortex (University of California-Berkeley, 2010). We can relate this study to Frank and his colleagues at the University of Pennsylvania, in terms of memory consolidation. In both experiments, the researchers concluded that we form memories while we are awake, while sleep is used as a method of consolidation.

On the other hand, research by Sejnowski and Destexhe (2000), discredits this hypothesis by proving that NMDAR is not the only factor in memory consolidation while sleeping. The work done by these researchers verifies that sleep spindles play a crucial role and is linked to long-term potentiation (enhanced signal between two neurons) by also triggering the flow of calcium. NMDAR is up-regulated during the awake cycle because of an increase in neuronal activity. However, researchers have found that in downscaling the net synaptic potentiation, or increase of NMDAR is counteracted by the slow wave activity during sleep. In addition, a study of sleep deprivation was conducted resulting in a synaptic depression and impaired LTP induction among the subjects, coinciding with the synaptic downscaling theory. Furthermore, by inhibiting the LTP, ripples of sleep spindles only come spontaneously and interrupted the normal process of memory consolidation and showing the relationship between sleep activity and synaptic depression. The data remains consistent suggesting that memory and sleep is only linked for the purpose of restoring synaptic depressions for new memory encoding. This proves that even though memory consolidation is initiated while being awake the process is not complete until the brain's activity is decreased and thus is provided with weak synaptic connections. This supports the first hypothesis by allowing memory formation to restore synapses during sleep and allow for encoding during the waking state. (Axmarcher et al.,2009 ).


         After a day of increased synaptic activity and high energy consumption, the brain spends a sleep cycle of weakening its synaptic connections and conserving energy for rejuvenation. Using Drosophila Melanogastor, researchers achieved an increase and decrease in proteins in the subjects consistent with the sleep-wake cycle and not the time of day. Similarly, gene manipulation in the circadian clock in fruit flies strengthens the downscaling theory by discovering sleep and synapse numbers were directly correlated. Lastly, NMDAR a molecule associated with memory formation is counteracted in the sleep cycle by slow wave formation refutes the strong synaptic connection hypothesis. Research in sleep and the strength of its synaptic connections need to be furthered studied before a complete conclusion can be drawn. In turn, further analysis will benefit sleep studies and change the way biologists look at why we sleep.


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