Some basic terms:

endogenous cycles	circadian	circannual
free-running	zeitgeber	phase advance/delay
SCN	period/time genes	retinohypothalamic path
pineal	melatonin	EEG/EOG/EMG
spindles	myoclonic jerks	hypnogogic/hypnopompic
paradoxical sleep

 Endogenous Rhythms and the Biological Clock (pp. 262-269)

1. If you have any doubts about the importance of biological rhythms in our lives, take a look at the following pattern which represents about 13 months of one person's life:

Figure from A. Borberly, Secrets of Sleep, 1986, p.171.

2. So...how is this 24 hr. rhythm regulated?  The figures below help explain how this is possible:
    

   Used by permission from: Kalat, J.W. Biological Psychology, 7th. Ed. Wadsworth Publ, 2001.  p. 285

   SCN cell activity when cultured in vitro [Figure adapted from the Herzog Lab, 2001]

    

3. OK, so we know that the SCN generates the circadian rhythms in most mammals.  But, how does it do so?  What's the mechanism?  What's all that stuff about period and timeless?  Here's another look at this from Jodi M
   
    

4. What is melatonin and what does it have to do w/ the SCN?  Here's an interesting update on how melatonin therapy has been used to improve sleep for the blind.
    

5.  Most introductory textbooks say that, in the absence of zeitgebers, the human circadian rhythm is approximately 25 hours in length.  Here is a description of an interesting case study that looked at this question.
    

6. On p. 268, your author notes that light continues to serve as a zeitgeber even for animals that are functionally blind.  Apparently, the light-sensitive mechanism that sends signals through the retinohypothalamic path to drive the internal clock is different from the one that produces vision.  Here's some old research on this question, and HERE's some more recent work on circadian mechanisms that adds a bit to how that might work.

  The Measurement of Sleep Stages  (pp.271-274)

1. Some basic terms you need to know:
   • polysomnograph
   • EEG
   • EOG
   • EMG

    

2. You can CLICK HERE for a summary of the various stages of sleep.  You'll need to know something about all these polysomnographs.  

    

3. What is Figure 9.10 all about?  Maybe this version makes more sense. 
    

4. Here's a good overview of this material from Joy H and another from Caridad M..
    

5. All of this has been on sleep in humans...here's some stuff on animals, thanks to Kristi B

Brain Mechanisms in Sleep  (pp.274-279) 

1. The following diagram shows many of the structures that are important in controlling arousal.   Be ready to talk about the critical structures and their functions, including:

   • pontomesencephalon

   • locus coeruleus

   • basal forebrain

   • histamine/antihistamines

   • adenosine

2. In addition to the mechanisms identified above, the shift from waking to NREM sleep involves several CNS mechanisms.  Be ready to discuss the role of each of the following:

• Core temperature and peripheral blood flow

• External stimulation

• Prostaglandins (inhibit histamine pathways of hypothalamus)

• Thalamocortial loop ®  delta wave oscillations

 

3. Classroom activity:  Each student is to select one of the structures or neurotransmitters above and do an in-class web search to find one new piece of information which adds to our understanding of these sleep/wake issues.  Be sure to evaluate the quality of the website.
    

4. The cycling between NREM ↔ REM during sleep.  If the SCN were the only factor influencing the sleep-wake cycle, then sleep patterns would be very simple:  with the approach of evening, arousal would slowly decline until we fell asleep.  Sleep would then gradually get deeper and deeper until a low point around 2:00 - 3:00 AM, at which time the cycle would reverse and arousal would gradually increase, eventually waking us up.  Arousal and alertness would then continue to increase till the high point is reached around 2:00PM, and the 24-hr cycle would start all over again:
   

   To some extent, this is what we see...SWS generally is most pronounced during the first half of the night (i.e. till about 2:00 or 3:00 AM if you go to bed at 11:00 PM) and then is increasingly replaced by REM (a more activated brain state) as morning approaches.
   
   Clearly, however, there is more to the sleep cycle than this simple 24-hr ebb and flow.  In particular, we experience significant variations in CNS arousal on a 90 minute cycle all night long.  This cycling between NREM to REM sleep also involves several CNS mechanisms.   Here are some relevant observations:

   • As early as 1949, Moruzzi and Magoun found that stimulation of locations in the reticular sytem in the brain stem led to activation of the cerebral cortex and arousal.  Sometimes, depending on the location stimulated, the arousal was accompanied by increases in muscle tone and the excitability of spinal reflexes (wake?).  Other locations produced arousal accompanied by  reduced muscle tone and inhibition of spinal reflexes (REM?).

   • When the Pons is surgically isolated from the cortex, then REM disappears and EEG recordings from the cortex show cycling only between wake and NREM!  On the other hand, when the Pons is surgically isolated from the spinal cord, then the cortex shows relatively normal Wake-NREM-REM cycling.

   • More recently, we have found that the Pons contains 2 groups of cells, called "REM-Off" and "REM-On" cells, which alternate about every 90 minutes.  When one of these sets of cells become active, they gradually turn themselves off while turning on the other set of cells.  Then, when the second set become active, they turn themselves off and while re-activating the first set.  This odd interaction leads to an alternating pattern of activity in the two sets of cells.

   • When the "REM-On" cells in the Pons are active, they seem to trigger a whole set of consequences:

     • Selected areas of the cortex show arousal at levels equal to waking, hence the very active EEG seen in REM

     • The primary motor cortex, where motor commands originate, becomes active, sending out lots of motor commands.  However, those commands are blocked as they pass down through the medulla on their way to the muscles, hence REM paralysis.  Damage to an area of the locus coeruleus (see the Figure above) eliminates REM paralysis and produces an odd phenomenon called REM movement disorder.

     • Sudden, periodic bursts of activity are triggered by some of the REM-On cells in the Pons.  These bursts then spread to the visual parts of the brain and to the muscles that move the eyes.  These bursts begin in the Pons and then quickly spread to the Lateral Geniculate Nucleus of the thalamus and then to the Occipital lobe (hence, PGO spikes).  In addition, REM's to the right or left are correlated w/ greater PGO activity in the right or left visual areas of the brain.  

     • During REM,  the following locations are especially active:

       • LGN and occipital cortex (vision)
       • vestibular nucleus (balance, orientation and movement)
       • primary motor cortex (muscle movements)
       • limbic system (emotions and memory)
       • occipital/parietal junction (language and vision)
     • During REM,  the following locations are relatively inactive or blocked:
       • motor command pathways in the brainstem...normally carrying motor commands to the muscles
       • dorsolateral prefrontal cortex  (working memory and the organization of behavior sequences)
       • sensory input:
         

   Finally, it should be noted that Nathaniel Kleitman (the father of sleep research) proposed that this 90 min. cycling is not unique to sleep; rather, Kleitman argued that it continues throughout the day;  its effects are just less noticable in the midst of all of our daytime activity.  He called this the Basic Rest-Activity Cycle (BRAC).   The existance and/or relevance of such an ultradian cycle is a bit controversial.  You can take a look a some recent evidence:  click here.

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Now: some basic sleep research issues and findings:

•  How do sleep patterns change across the lifetime?

   

• Is sleep necessary?  If so, how much, and what function(s) does it serve?  The obvious way to get at this issue is to look at what happens when we don't sleep.   Another approach is to look at data like those in Figure 9.17.  Are you convinced?  If you are, then check this out.

   

• How about REM sleep; is it necessary, and if so, why?  Selective deprivation leads to:

  • reduced REM latency, intrusions of REM-like phenomena during the day, and REM rebound during recovery sleep (REM pressure)

  • mild psychological disturbances, including anxiety, irritability, and difficulty concentrating. 

  • in rats, REM deprivation has been reported to produce hyper-sexuality
     

• Relatively few NREM deprivation studies because of methodological problems
   

• Before finishing, let's look at one proposed model for understanding sleep by a widely respected French researcher.  (Note: to be fair to Borberly, he has modified and refined this model, but the earlier, simpler version below will serve our needs)
  

  • The primary purpose of this model is to account for the overall patterns of sleep and wakefulness that are seen under a variety of conditions.  One way to measure wakefulness is the MSLT.   So, does this model adequately account for the MSLT data we saw earlier? 

  • Also, based on what we read about Dava Sobel's experience in a free-running environment, can you identify one additional factor that influences sleep which isn't included in this model?
    
     

• Sleep disorders...

  • here's some info on sleep walking, thanks to Angie H

  • here's something on narcolepsy from Cathy G

  • and here's something on apnea from Sarah S.

  • finally, here's a site on insomnia from Ben L.