tomh.bbs@shark.cs.fau.edu (Tom Holroyd) (05/01/91)
>>>One can theorize based on comparative phylogeny, but the functional >>>experiments of knockout and overexpression (i.e. with carbachol >>>injection into the pontine midbrain) haven't suggested any roles for >>>REM sleep in the adult brain. Such experiments are only now being >>>attempted in the developing brain (i.e. recent experiments by Gerry >>>Vogel). >> >>There is no such thing as the pontine midbrain. The midbrain and the >>pons are two different things. > >Come on, Tom... He may either be using the terminology a bit sloppily, >or it may be that some people juxtapose the words as such to denote >nuclei that span the two gross regions. Note the title of the paper I >cited... How would you try to translate "pontomesencephalic"? >>Deprivation of REM sleep causes death. OK, sorry, my mistake. Mr. Van Gelder does have a good point. I got my information from a friend and just posted without checking.. I have checked now. Again, sorry for the knee-jerk post. I should know better. >I wasn't familiar with this, so I just did a medline search. I >suspected that Tom was wrong--that although there may be dire >consequences to suppressing REMS in an anatomically "normal" animal, >REMS may disappear in some pathologies without ultimately leading to >death. My medline search turned up (among other things): > > Webster, HH, and Jones, BE. (1988). "Neurotoxic Lesions of the > Dorsolateral Pontomesencephalic Tegmentum Cholinergic Cell Area > in the Cat: Effects on Sleep-Waking States", Brain Res. > 458(2):285-302. > >I haven't read it, but from what I saw in the abstract, REMS was >always abnormal after these lesions, and it usually disappeared >altogether immediately after the lesion. The animals went for up to a >month (if I recall that right) without REMS, but there was no mention >in the abstract that it ever disappeared permanently. I doubt that >I'll take the time to pull up the paper--perhaps someone else (Russ?) >can tell us more? OK, this time with references: Deprivation of sleep (not only REMS) causes severe states of exhaustion and death (1). The REM deprivation literature, however, does not support that the loss of REM causes death (2). I was wrong about this. However, the most common methods of REM deprivation (flower pot technique: place rat on top of an inverted flower pot in a pan of water. When rat enters REM, muscle atonia cause rat to fall into water, waking it up) also causes a loss of deep sleep. More on this later. Also, Rechtschaffen has seen cases of long term REM deprivation leading to death (3) but this may be the result of "a relatively slow process of debilitation," and not specifically the result of loss of REMS. REM can be suppressed with various drugs (this addresses Mr. Van Gelder's excellent point). Crick and Mitchison (4) have noted that *no* obvious behavioral changes result from the elimination of REMS using monoamine oxidase inhibitors (MAOIs). However, MAOIs alter the total pattern of sleep - not only do they suppress REMS, but slow-wave sleep is also suppressed (5). If one of the functions of REMS is to periodically activate the cortex to break up cyclic modes (parasitic modes?) then loss of deep slow wave sleep would eliminate the need for REM sleep. I don't know of any drug that selectively eliminates REMS without altering sleep in some other way. As for the lesion study cited above, I don't know, but you can bet I'll check it out. The original idea was the observation (from a mathematical point of view, here) that slow wave sleep was limit cycle type behavior. From the early studies by Jouvet where the brainstem was transected rostrally, one gets the idea that without brainstem input, the cortex sort of naturally oscillates. From the math of limit cycles, you can see that once in a limit cycle, you generally can't get out with a small perturbation. A chaotic attractor is much more sensitive to small perturbations. So a cortex in slow wave sleep is less sensitive to input, and harder to arouse, than a cortex being activated by the brainstem. So I thought that the desychronized EEG (active cortex) during REM was the brain's way of making sure that the cortex doesn't get trapped in a limit cycle. I mentioned this to Dr. Vertes (a neuroscience guy and sleep researcher here at FAU), and found out that he had already published a paper along these very lines (6)! He essentially says that the brain is incapable of tolerating long continuous periods of inactivity. This theory appeals to me because of the mathematical model I mentioned above (although Vertes doesn't mention any math model in his paper). (1) Rechtschaffen, A., M.A. Gilliland, B.M. Bergman and J.B. Winter. Physiological correlates of prolonged sleep deprivation in rats. Science 221: 182-184, 1983. (2) Vogel, G.W. A review of REM sleep deprivation. Arch. Gen. Psychiatry 32: 749-761, 1975 (3) Kushida, C., B. Bergman, C. Everson, J. Winter and A. Rechtschaffen. Paradoxical sleep deprivation in the rat: I. Physiological effects. In: Sleep Research, vol 13, edited by M.H. Chase, W.B. Webb and R. Wilder-Jones. Los Angeles: Brain Information Service/Brain Research Institute, UCLA, 1984, p. 190. (4) Crick, F. and G. Mitchison. The function of dream sleep. Nature 304: 111-114, 1983. (5) Cohen, R.M., D. Pickar, D. Garnett, S. Lipper, J.C. Gillin and D.L. Murphy. REM sleep suppression induced by selective monoamine oxidase inhibitors. Psychopharmachology (Berlin) 78: 137-140, 1982. (6) Vertes, R.P., A Life-Sustaining Function for REM Sleep: A Theory, Neuroscience & Biobehavioral Reviews, 10(4), 371-376, 1986. Tom Holroyd Center for Complex Systems Florida Atlantic University tomh@bambi.ccs.fau.edu My thanks also to Dr. Vertes for supplying me with the references above.