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The Suppression of Wakefulness
The first and most important question we must answer is this : Does
the nervous system possess a specific sleep-producing mechanism ? In other
words, should we not rather confine our research to the operations of
the mechanism that keeps us awake ? Kleitman has put the issue very clearly
; he observes that to say one falls asleep or is put to sleep is not the
same as saying one ceases to stay awake. The first statement implies that
an active mechanism suppresses the state of wakefulness-a mechanism analogous
to applying the brakes in an automobile, The second statement implies
that the wakefulness-producing mechanism simply stops operating a situation
analogous to removing the foot from the accelerator. Thus the mechanism
responsible for sleep would be negative or passive, not active. Now, it
has been known for nearly two decades that the brain contains a center
specifically responsible for main aining wakefulness. This was discovered
by H. W. Magoun of the U.S. and Giuseppe Moruzzi of Ital.y, working together
at Northwestern University [see "The Reticular Formation," by
J. D. French; SCIENTIFIC AMERICAN, May, 1957]. They named this center,
located in the midbrain, the reticular activating system (RAS). Stimulation
of the RAS center in a slumbering animal arouses the animal; conversely,
destruction of the center causes the animal to go into a permanent coma.
To explain normal sleep, then, we must find out what process or mechanism
brings about a deactivation of the RAS for the period of sleep.
On the basis of the known facts about the RAS there seemed at first
no need to invoke the idea of a braking mechanism to account for deactivation
of the system. The Belgian neurophysiologist Frédéric Bremer
suggested that the RAS could simply lapse into quiescence as a result
of a decline of stimuli (such as disturbing noise) from the surroundings
[see "Sleep," by Nathaniel Kleitman; SCIENTIFIC AMERICAN, November,
1952].
Several years ago, however, explorations of the brain by the Swiss neurophysiologist
W. R. Hess and others began to produce indications that the brain might
contain centers that could suppress the activity of the RAS. In these
experiments, conducted with cats, the cats fell asleep after electrical
stimulation of various regions in the thalamus and elsewhere or after
the injection of chemicals into the cerebrum. Interesting as these findings
were, they were not very convincing on the question at issue. After all,
since a cat normally sleeps about two-thirds of the time anyway, how could
one be sure that the applied treatments acted through specific sleep inducing
centers ? Moreover, the experiments seemed to implicate nearly all the
nerve structures surrounding the RAS, from the cerebral cortex all the
way down to the spinal cord, as being capable of inducing sleep. It was
implausible that a sleep-inducing system could be so diffuse. Nevertheless,
in spite of all these doubts, the experiments at least pointed to the
possibility that the RAS might be influenced by other brain centers. Moruzzi
and his group in Ital.y proceeded to more definitive experiments. Seeking
to pin down the location of a center capable of opposing the action of
the RAS, they focused their search on the lower part of the brainstem.
They chose a site at the middle of the pons in front of the trigeminal
nerve, and with cats as subjects they cut completely through the brainstem
at that point. The outcome of this operation was that the cats became
insomniac : they slept only 20 percent of the time instead of 65 per cent
! The brain cortex showed the characteristic electrical activity of wakefulness
(fast, low-voltage activity), and the eye movements also were those of
a wakeful animal pursuing moving objects. The experiments left no doubt
that the cut had disconnected the RAS from some structure in the lower
part of the brainstem that normally exercised control over the waking
center. It was as if a brake had been removed, so that the RAS was essentially
unrestricted and kept the animal awake most of the time. The new evidence
leads, therefore, to the conclusion that sleeping is subject to both active
and passive controls. The active type of control consists in the application
of a brake on the RAS by some other brain structure or structures; the
passive type corresponds to a letup on the accelerator in the RAS itself.
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