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Just one night without sleep can increase the amount of the chemical
dopamine in the human brain, according to new imaging research in the
20 August issue of The Journal of Neuroscience. Because drugs that
increase dopamine, like amphetamines, promote wakefulness, the
findings offer a potential mechanism explaining how the brain helps
people stay awake despite the urge to sleep. However, the study also
shows that the increase in dopamine cannot compensate for the
cognitive deficits caused by sleep deprivation.

'This is the first time that a study provides evidence that in the
human brain, dopamine is involved in the adaptations that result from
sleep deprivation,' said Nora Volkow, MD, director of the National
Institute on Drug Abuse, who led the study.

Volkow and colleagues found that in healthy participants, sleep
deprivation increased dopamine in two brain structures: the striatum,
which is involved in motivation and reward, and the thalamus, which is
involved in alertness. The researchers also found that the amount of
dopamine in the brain correlated with feelings of fatigue and impaired
performance on cognitive tasks.

'These findings suggest dopamine may increase after sleep deprivation
as a compensatory response to the effects of increased sleep drive in
the brain,' said David Dinges, PhD, at the University of Pennsylvania
School of Medicine, an expert unaffiliated with the study. 'The extent
to which this occurs may differentiate how vulnerable people are to
the neurobehavioural effects of sleep loss,' Dinges said.

The researchers studied 15 healthy participants who were either kept
awake all night or allowed a good night's sleep. Researchers tested
the same participants in both conditions. On the morning of the study,
participants rated how tired they were and did cognitive tasks testing
visual attention and working memory.

The researchers used the imaging technique positron emission
tomography to study the changes in the dopamine system that occur with
sleep deprivation. Compared to well-rested participants,
sleep-deprived participants showed reduced binding of a radiolabelled
compound ([11C]raclopride) that binds to dopamine receptors in the
striatum and thalamus. Because raclopride competes with dopamine for
the same receptors, decreased raclopride binding indicates increased
levels of dopamine, according to the study authors.

Although decreases in raclopride binding could also indicate a
reduction in the number of dopamine receptors, these findings are
consistent with prior research implicating increased dopamine levels
in wakefulness. For example, some stimulants that prevent sleep, like
amphetamines, increase dopamine in the brain, and sleepiness is common
in people with Parkinson's disease, which kills dopamine neurones.

The rise in dopamine following sleep deprivation may promote
wakefulness to compensate for sleep loss. 'However, the concurrent
decline in cognitive performance, which is associated with the
dopamine increases, suggests that the adaptation is not sufficient to
overcome the cognitive deterioration induced by sleep deprivation and
may even contribute to it,' said study author Volkow.

Future research will examine the long-term effects of chronic sleep
disturbances on dopamine brain circuits.

Source: Society for Neuroscience

http://www.sciencecentric.com/news/article.php?q=08082310

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