The Joy of Sleep Deprivation

At Stuyvesant, it's not uncommon for students to sacrifice their sleep to finish projects or study for their exams. Those who pull an all-nighter experience a mix of both physical fatigue and mental giddiness. This feeling is often described as “tired and wired.” While the root cause of the combined physical exhaustion and mental excitement was once unclear, recent research by neurologists at Northwestern University may have uncovered what produces this distinctive sensation.  

It is common knowledge that a good night’s sleep is important to functioning when awake. Sleep keeps us aware of our surroundings and allows our brains to work properly. The ability to feel alert throughout the day is linked to dopamine, a hormone released during sleep that stimulates feelings of happiness and pleasure. Dopamine is responsible for maintaining an individual's energy levels until the body is ready to sleep, with higher levels of dopamine indicating heightened levels of wakefulness. Moreover, dopamine is important in maintaining mental well-being throughout the day. Previous research has shown that lower levels of dopamine in the brain are associated with higher rates of depression, a severe mental disorder that can negatively affect how one feels, thinks, or acts. 

Chronic sleep loss or prolonged sleep deprivation over a period of two or more days would disrupt the normal release of dopamine, lowering the amount released. This disruption occurs from alterations in the circadian rhythm, a cycle controlled by the sleep schedule that regulates hormones like dopamine and their release from the body. Hence, chronic sleep can be extremely detrimental to the body, increasing an individual's likelihood of having depression-like symptoms throughout the day. 

While these consequences may be true in cases of chronic sleep loss, an experiment performed by Dr. Yevgenia Korozorvitisky and Dr. Mingzheng Wu at Northwestern University suggests that acute, or temporary, sleep loss may actually temporarily increase dopamine levels and alleviate depression symptoms for several days. Kozorovitskiy and her team conducted an experiment to observe behavior and brain activity in mice who underwent acute sleep deprivation—a period of one to two days during which the mice did not sleep. After the first night, the researchers observed that the mice became more aggressive, hyperactive, and hypersexual. Then, using dopamine sensors, the researchers measured the activity of dopamine neurons in the four regions of the brain responsible for dopamine releases: the prefrontal cortex, nucleus accumbens, hypothalamus, and dorsal striatum. 

  They discovered that mice experiencing sleep deprivation had higher dopamine levels in the prefrontal cortex, nucleus accumbens, and hypothalamus when compared to mice that received a sufficient eight hours of sleep. In order to pinpoint the exact area of increased dopamine levels, the researchers systematically silenced dopamine reactions in these three brain regions by using proteins that inhibit dopamine release from the other areas of the brain. Through this process, researchers discovered that dopamine levels significantly decreased when the medial prefrontal cortex was silenced. Thus, they concluded that the nucleus accumbens and hypothalamus have less involvement in dopamine excretion and instead have other effects on the body during periods of sleep deprivation. 

The researchers noted that increased dopamine levels in mice lingered for several days, indicating that a process known as synaptic plasticity was taking place in the brain. Synaptic plasticity is the ability of the neurons to modify connections to other neurons, essentially remodeling the brain to follow different patterns of brain function. In this case, synaptic plasticity would allow the prefrontal cortex to continuously excrete higher amounts of dopamine over a longer period of time. While closely observing individual neurons in the prefrontal cortex, researchers discovered that neurons formed tiny protrusions called dendritic spines, highly plastic features that change in response to brain activity. This discovery affirms the theory of synaptic plasticity in the prefrontal cortex because when the researchers used a genetically encoded tool to disassemble the spines, the dopamine levels were reversed to resemble those found in the mice who received a full night of sleep.

Though scientists are unsure why sleep loss causes dopamine increases in the brain, some speculate that humans have developed this way for evolutionary reasons. However, routinely losing sleep is detrimental, as the body would eventually catch up to the disordered circadian cycle and the irregular secretion of hormones throughout the day, resulting in overwhelming fatigue. 

While the results of the experiment do not lead to any affirmative conclusions about the direct impact of sleep deprivation on depression, the acquired knowledge opens up numerous possibilities for treating depression. As discovered in the procedure, brain regions such as the medial prefrontal cortex produce more significant amounts of dopamine and thus play a larger role in maintaining mood throughout the day. With this knowledge, researchers can target the development of drugs that focus on dopamine release in the areas that heavily regulate mood. Hopefully, in the future, further experiments can be conducted to discover more about this debilitating mental disorder and its relationship to sleep.