REM sleep: a new perspective?

John Booth john.booth at
Fri Feb 4 17:33:10 EST 2000

Dear Group,

I am a medical student preparing to take my 1st BM Part II exams. I
specialise in neuroscience and would be interested to hear some feedback on
a theory I have developed regarding the basis of sleep, and in particular
REM (paradoxical) sleep.

As you may well be aware, REM or dream sleep is currently explained in two
opposing theories: the first ascertains that the basis of REM sleep (during
which the cerebral cortex is paradoxically active as seen on the EEG) is to
'imprint' memories which have been laid down during the preceding day. The
second, as put forward by Francis Crick, purports that REM sleep embodies
the exact opposite, a period of 'unlearning' where the cerebral cortex
removes the 'dead ends' that are a natural consequence of cortical
plasticity. Crick's theory has limited evidence in support of it (eg
dolphins and anteaters do not sleep and have exceptionally large cerebral
cortices to accommodate the redundant circuitry) but the weight of current
evidence lies in favour of the former theory. For instance, electrical
recording experiments on rats have shown that the same patterns of cortical
and hippocampal activity abound during REM sleep as were being experienced
during the day.

Before detailing my theory, it is important to note that sleep in general
has been appreciated for some time now as a period during which the body
rectifies neurotransmitter balance, removes toxins and adjusts metabolic

What precipiated my new hypothesis on REM sleep was the simple observation
that undergraduates (of whom many surround me) claim to 'dream more' amd
more vividly after a night of alcohol consumption than during a normal
night's sleep. Of course, without the necessary EEG equipment, time and
willing subjects I cannot prove this claim, but if it is true, I feel that
it could be explained as follows.

I believe that in the same way as classically autonomic systems such as the
CV and respiratory systems can supposedly be driven by the cortex (eg
cortical CV set during exercise), so too can human basal metabolism be
driven by the telencephalon (presumably via the ANS). It would make sense to
see a degree of coupling between cortical activity and metabolic activity
since generally the body is more active when the mind is active. Assuming
the existence of such a coupling, one can turn now to REM sleep, periods of
sleep where the cortex is paradoxically active: could it be that this
cortical activity is efficiently driving bursts of metabolism to restore the
body's chemical equilibrium? Two pieces of evidence lie in my favour: first
is the effects of alcohol consumption before sleep. After alcohol, liver
metabolism increases in an attempt to detoxify the body, and so the
increased REM sleep represents an increased frequency of cortically-coupled
bursts of metabolism to facilitate the detox (?REM type discharges probably
have to be incorporated in sleep because either the cortical discharges or
metabolic sequelae are too vigorous to be tolerated in the waking phase.)
Second, the rat studies used to corroborate the 'imprinting of memories'
could merely be a reflection of the fact that in general only the most
facilitated cortical circuits (most-facilitated because they have only
recently been layed down) 'light up', during REM sleep, as some subcortical
structure attemts to stimulate the cortex.

As I said, I would love to have some feedback on these ideas.

John Booth. Oxford 2/2000.

More information about the Neur-sci mailing list