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Sleep research shows that
certain regions of the brain play critical roles in sleep. The
brainstem, the portion of the brain just above the spinal cord, is
critical in REM sleep control, while the forebrain is particularly
important in NREM sleep control.
REM sleep is generated by a region in the brainstem, called the pons,
and adjacent portions of the midbrain. Researchers have found that
chemical stimulation of the pons will induce very long periods of
REM sleep, while damage or injury to this brain region can greatly
reduce or even prevent REM sleep. Animal studies have found that
some neurons within the pons and midbrain are active only in REM
sleep while other neurons in this region are entirely inactive only
during REM sleep. Together, these neurons control muscle tone and
other aspects of REM sleep. In REM sleep, most muscles in the body
are turned off. This lack of muscle tone, called atonia, is
particularly complete in the muscles of the back, neck, arms, and
legs. Less affected are the muscles that move the eyes and the
muscles responsible for breathing.
The combined effect of the sleep-active and sleep-inactive neurons
explains why sleepers do not physically act out the vivid dreams
they have during REM sleep and instead only twitch or make small
movements. Humans with malfunctioning REM sleep-active and REM
sleep-inactive systems thrash around in their sleep, often punching
their bedmates or hurting themselves as they act out their dreams.
The neurons most critical to NREM sleep control are in the basal
forebrain, the region of the brain lying in front of the
hypothalamus. Researchers have found that people who have suffered
damage or injury to the neurons in the basal forebrain have
difficulty falling and staying asleep. Animal studies have shown
that this area contains neurons that become most active before and
during sleep. Many of these neurons are activated by heat, which
explains how a warm bath or a hot day at the beach causes
sleepiness. |
