tomh.bbs@shark.cs.fau.edu (Tom Holroyd) (04/26/91)
1. Echidnas have no desynchronized EEG during sleep (I don't know about eye movements, but that's not the point; I'm interested in the cortical activity). 2. They have a very large (proportionaly) neocortex, particularly frontal. In humans: Deep sleep EEG is synchronized. Periodically, during sleep, the cortex becomes active (desynchronized) accompanied by rapid eye movements (REM), PGO spikes, etc. (Hippocampal theta, too, I think). Synchronized EEG is a lower dimensional state than desynchronized EEG. The system doesn't wander around much, it mostly stays where it is, or drifts around slowly. The active cortex, on the other hand, is high-dimensional - there are many more degrees of freedom available to the system. REM sleep may be the brain's way of ensuring that we don't get "stuck" in the lower-diemsional synchronized state during deep sleep. Periodic bursts of activity kick the system out of the relatively small limit- cycle attractor. Patients in coma, for example, do not have REM sleep, and measurements of their EEG dimension show an even more synchronized state than for normal deep sleep. They are "stuck." Echidnas may not have desynchronized sleep because their larger neocortex gives them the added dimensionality they need to make it through the night - but this would be a very inefficient way to do it. Periodic desynchronizing bursts would be better, since the dimensionality can be raised higher and faster. Some added thoughts: The neurons involved in the cyclic behavior would adapt themselves to the activity level, becoming less active in the process. This would make it even more difficult to get out of the low D state. The stimuli that normally cause waking, including the internal ones, are merely perturbations of a vastly larger system. These signals would be enough to cause cortical activation if the brain isn't in an abnormally low D state. REM sleep activity in the cortex keeps the pathways sensitive to stimulation, so when morning comes around, the various stimuli wake you up. This doesn't explain REM rebound or why REM deprivation is bad. Presumably, waking the person should activate the cortex, taking the place of REM. Waking activation may be ineffective however, due to the lack of modulatory influences present during sleep (such as, perhaps, theta rhythm). Comments? Tom Holroyd Center for Complex Systems Florida Atlantic University tomh@bambi.ccs.fau.edu
vangeldr@cmgm.stanford.edu (Russ Van Gelder) (04/27/91)
A couple of functional questions about REM sleep: 1. What is the phenotype of continuous pharmacologic suppression of REM sleep, as is seen in patients on long-term antidepressants. I believe that, aside from the antidepressant effect, in humans, there is no real phenotype. 2. What is the phenotype associated with lesions of the pedunculo- pontine tegmentum? Barbara Jones has performed these lesions in cats, resulting in a complete or almost complete loss of REM sleep. The animals seem fine. 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). Russ (vangeldr@cmgm.stanford.edu)
rowe@pender.ee.upenn.edu (Mickey Rowe) (04/29/91)
In article <cwP116w163w@shark.cs.fau.edu> tomh.bbs@shark.cs.fau.edu (Tom Holroyd) writes: >In humans: ... >Deep sleep EEG is synchronized. Periodically, during sleep, the >cortex becomes active (desynchronized) accompanied by rapid eye >movements (REM), PGO spikes, etc. (Hippocampal theta, too, I think). etc. ... >Synchronized EEG is a lower dimensional state than desynchronized >EEG. The system doesn't wander around much, it mostly stays where >it is, or drifts around slowly. The active cortex, on the other hand, >is high-dimensional - there are many more degrees of freedom available >to the system. >Comments? I'm forwarding your post to a friend of mine who works in Adrian Morrison's lab... Hopefully I can get her to respond to this since she will likely give a better informed opinion. In the meantime you'll have to settle for me :) (though I'd also suggest that you might want to repost your original article to bionet.neuroscience). I'm guessing from your post that you feel that the purpose of sleep is to put cortex into a state of low activity. If you feel that this is in order to give neurons a chance to rest, I have to tell you that I've never met *anyone* who took that idea seriously. Frankly, I think that even if Francis Crick is a bit removed from reality, his ideas about the purpose of REMS seem a bit more likely. Current consensus amongst sleep researchers is that sleep is a very active period for nervous systems, and I suspect that you'd be hard pressed to find any of these people to agree that REMS exists to jolt the inactive brain closer to a waking state. There's quite a bit of literature on what's happening in sleeping brains if you'd like some names to look into. Forgive me for assuming that you might not be familiar with other ideas, but your analysis appears to me to be a bit shy on the side of biology... >Tom Holroyd >Center for Complex Systems >Florida Atlantic University >tomh@bambi.ccs.fau.edu Mickey Rowe (rowe@pender.ee.upenn.edu)
tomh.bbs@shark.cs.fau.edu (Tom Holroyd) (04/29/91)
> suggest that you might want to repost your original article to > bionet.neuroscience). I'm guessing from your post that you feel that > the purpose of sleep is to put cortex into a state of low activity. I'd say that, in the absense of input, the natural state of the cortex is low activity, synchronized. The cortex needs input to desynchronize it. There is reduced input during sleep, hence more oscillatory behavior. > active period for nervous systems, and I suspect that you'd be hard > pressed to find any of these people to agree that REMS exists to jolt > the inactive brain closer to a waking state. From what I've read, it's difficult to get sleep researchers to agree. :-) I'm speaking from the point of view of dynamical systems. If the cortex remains in a limit cycle state for too long, it may be difficult for it to escape. This implies facilitation of the pathway. On the other hand, if the pathway habituates, it may cause a shift to another, related limit cycle, with no more dimension than the first. I have gotten a response from someone who said there was only one experiment done to show that echidnas have no REM sleep, and the animal may have been hibernating, not sleeping! This brings up the question of whether hibernating animals in general have REM sleep or not. I don't know. Tom Holroyd Center for Complex Systems Florida Atlantic University tomh@bambi.ccs.fau.edu
rowe@pender.ee.upenn.edu (Mickey Rowe) (04/30/91)
In article <619614w163w@shark.cs.fau.edu> tomh.bbs@shark.cs.fau.edu (Tom Holroyd) writes: >I'd say that, in the absense of input, the natural state of the cortex >is low activity, synchronized. Hmmmmmm... In the first place I'd doubt that sleep represents an absence of input... Just because you don't remember the sensory experiences that you have when you're asleep doesn't mean that they're not there. I live in a city near busy streets, and I assure you that my ears are getting plenty of stimulation regardless of my conscious state. It seems to me that input is not absent, it's just ignored. In the second place, I'm not so sure that I would agree with this natural state. Perhaps you could make a case for this from the cerveaux isole or encephale isole studies, but I wouldn't put much credence in it if you didn't have other evidence. You might also want to look at Ron Harris-Warwick's stuff about modulation of oscillatory circuits. Assuming that the periodic activity in EEG's comes from cyclic activity amongst groups of neurons, his work could be relevant. He's studying the stomatogastric ganglion of crustaceans, and showing that this single network of about six types of cells has vastly different properties depending on what types of neurotransmitters he puts on them. Which cells are active, what the phase relationships are between different types of cells etc. changes pretty dramatically with small concentrations of neurotransmitters. I would tend to argue that there is no "natural" state of a group of neurons... > The cortex needs input to desynchronize it. >There is reduced input during sleep, hence more oscillatory behavior. My feeling is that your causality here is completely uncalled for. In fact Charlie Gray's work indicates that visual input causes oscillatory behaviour in area V1, and that oscillatory behavior as a response to input may be the manner in which different attributes of a single stimulus are grouped together. Granted these oscillations are much faster than theta waves... >From what I've read, it's difficult to get sleep researchers to >agree. :-) Oh, I'm sure that half of them would disagree with that :^) >I'm speaking from the point of view of dynamical systems. If the cortex >remains in a limit cycle state for too long, it may be difficult for >it to escape. I'm afraid that I don't completely understand your terminology, but I guess that the missing piece for me here is an implied suggestion that the purpose of sleep is to put cortex into this limit cycle state. What would the advantage of that be? (This is a real question, not a challenge.) >I have gotten a response from someone who said there was only one >experiment done to show that echidnas have no REM sleep, and the >animal may have been hibernating, not sleeping! This brings up >the question of whether hibernating animals in general have REM >sleep or not. I don't know. If they don't I think that your idea about why REMS exists is on pretty shaky ground... >Tom Holroyd >Center for Complex Systems >Florida Atlantic University >tomh@bambi.ccs.fau.edu Mickey Rowe (rowe@pender.ee.upenn.edu)
tomh.bbs@shark.cs.fau.edu (Tom Holroyd) (05/01/91)
vangeldr@cmgm.stanford.edu (Russ Van Gelder) writes: >A couple of functional questions about REM sleep: > >1. What is the phenotype of continuous pharmacologic suppression of >REM sleep, as is seen in patients on long-term antidepressants. I >believe that, aside from the antidepressant effect, in humans, there >is no real phenotype. I don't understand the question. Phenotype? That has to do with development, right? I don't know about the EEG of patients on anti-depressants. >2. What is the phenotype associated with lesions of the pedunculo- >pontine tegmentum? Barbara Jones has performed these lesions in >cats, resulting in a complete or almost complete loss of REM sleep. >The animals seem fine. Deprivation of REM sleep causes death. A dead cat does not seem fine to me. >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. Again, deprivation of REM sleep causes death. This suggests that it does do *something*. Tom Holroyd & Bill Fortin Center for Complex Systems Florida Atlantic University tomh@bambi.ccs.fau.edu
rowe@pender.ee.upenn.edu (Mickey Rowe) (05/01/91)
In article <q39812w163w@shark.cs.fau.edu> tomh.bbs@shark.cs.fau.edu (Tom Holroyd) writes: >vangeldr@cmgm.stanford.edu (Russ Van Gelder) writes: > >>2. What is the phenotype associated with lesions of the pedunculo- >>pontine tegmentum? Barbara Jones has performed these lesions in >>cats, resulting in a complete or almost complete loss of REM sleep. >>The animals seem fine. > >Deprivation of REM sleep causes death. A dead cat does not seem fine >to me. 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? >>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"? >Again, deprivation of REM sleep causes death. This suggests that it >does do *something*. I would tend to agree that REMS has a purpose throughout life, but even if animals that are deprived of REMS do die (I'd like a reference to this, since the only place I've actually heard that such experiments were ever taken to that outcome was Star Trek The Next Generation), that does not mean that it is the lack of REMS that caused their death. The two mechanisms that I can recall that people have used to deprive animals (or people) of REMS are carbachol injections, or waking the subject when the EEG indicated that REMS was about to occur. If either of these types of experiments lead to the death of the subject, you'd be hard pressed to convince me that the lack of REMS was the only thing that could have caused that death. >Tom Holroyd & Bill Fortin >Center for Complex Systems >Florida Atlantic University >tomh@bambi.ccs.fau.edu Mickey Rowe (rowe@pender.ee.upenn.edu)
isaak@imagen.com (mark isaak) (05/01/91)
In article <q39812w163w@shark.cs.fau.edu> tomh.bbs@shark.cs.fau.edu (Tom Holroyd) writes: >Deprivation of REM sleep causes death. In one of my psychology courses, I heard about an Israeli soldier who, due to an injury (shrapnel in the brain), lost all capacity for REM sleep. He was apparently doing fine otherwise. Sorry, I have no references for this. -- Mark Isaak imagen!isaak@decwrl.dec.com or {decwrl,sun}!imagen!isaak "Convictions are more dangerous enemies of truth than lies." - Nietzsche