Restorative Effects of Sleep

As mentioned above, sleep problems are common in psychiatric disorders. Again, the most prominent example is the tendency of depressed individuals to sustain sleep poorly and to wake in the middle of the night, partly because their pituitary adrenal stress waking/alarm system become active much earlier than normal (Kryger et al., 2000). Other features include an excessively rapid entry into the REM phase after sleep onset. Since sleep recruits endogenous antistress mechanisms and depression impairs quality sleep, the sleep problems of depression may tend to perpetuate ongoing problems. Although there is likely some truth to that hypothesis, such a problem would have to reside within the disruption of SWS rather than REM. A remarkable finding is that REM sleep deprivation is a fairly effective short-term antidepressant, and practically all of the pharmacological antidepressants are excellent REM sleep inhibitors (Kryger et al., 2000). One could construct a provisional explanation by supposing that the failure to dissipate emotional energies during REM might help make them available for waking activities, but no test of such an idea is available. An appropriate experiment would require some way of measuring these types of neuropsychological energies.

One way this has been done in animals is to see how specific emotional systems operate as a function of the REM sleep process. This has been achieved by surgically dampening REM atonia, which normally keeps animals recumbent during the supposed emotional episodes of their dreams. In such animals, the various instinctual-emotional action programs, which are presumably active in dreams, are now expressed physically—including predatory stalking, rage and fearful behaviors, and grooming. This informs us that emotional processes are, in fact, aroused in the dreams of other animals, which is consistent with the finding of high levels of emotionality in human dreams, as well as the fact that the limbic system tends to exhibit selective arousal during REM sleep (Nofzinger et al., 1997).

Another way to get at the relationship between REM and emotions would be to take one emotional system and study its dynamics as a function of REM deprivation. This has been done with self-stimulation of the lateral hypothalamus (the SEEKING system described in Chapter 1). This emotional substrate is more responsive in REM-deprived rats since they self-stimulate more. Even more remarkably, rats that are allowed to self-stimulate (i.e., to use up the energy in this system) during the course of the REM deprivation do not exhibit the type of compensatory REM sleep rebound (i.e., post-deprivation elevations in REM) that is normally seen in deprived animals. A similar absence of rebound following REM deprivation is also seen in schizophrenic patients, suggesting that their waking activities may be depleting the neuropsychological emotional energies that normally build up when organisms are not allowed to undergo REM sleep. One way to view these findings is that REM deprivation increases dopamine arousal in the brain, while REM sleep diminishes it. From this perspective, it is interesting that dopamine facilitators generally brighten mood, even to the point of euphoria, and some have found a place as antidepressants as well as anti craving medications for nicotine addiction (bupropion: Wellbutrin or Zyban, respectively).

Although there are many theories concerning the functions of dreaming, none has sufficient support to be well accepted (for summaries of controversies, see the special issue of The Behavioral and Brain Sciences, 2000, vol. 23(6), pp. 793-1121). In contrast, there are fewer theories about the functions of SWS, but the characteristic secretions of growth hormone that occur at the onset of SWS strongly suggest that at least part of the story is body restoration. Further, since one is truly unconscious during deep SWS, and cerebral metabolism is markedly reduced (Nofzinger et al., 1997), one would expect that there is abundant rejuvenation of brain functions during this phase of sleep. Attempts to characterize the changes in gene expression that accompany sleep indicate that about 0.5 percent of genes are expressed differentially in the cerebral cortex across phases of sleep, and those that are up-regulated during sleep tend to be presently unidentified genes (Tononi and Cirelli, 2001). This gives us very little leeway for any major interpretations, except to say that many important things are happening.

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