 Originally Posted by arby
Ah, cool. When you do the study, I'll help any way that I can. Need any personnel accounts or anything and i'll try my best =) Then be sure to post your results here =)
I would wonder what actually does trigger the return to consciousness without interruption however. If it is a chemical, what would happen if that chemical were not present in your day? Chemically speaking, should there be a difference between waken by an alarm and not?
What wakes us up:
The ascending reticular activating system:
Early on, someone noticed that if the midbrain of a cat was transected (at point A, below), the cat fell into a coma - their EEG became permanently synchronized. This finding alone is not too surprising. However, if the transection was made down in the medulla (at point B), the cat was only paralyzed, not comatose. The most surprising phenomenon was that if the rostral stump of the transected midbrain was electrically stimulated (blue arrow), the cat "woke up" - according to its EEG.

From these experiments it was concluded that there was some pathway originating in the pons or midbrain that ran forward into the cerebrum and stimulated wakefulness. The pathway was thought to originate with a group of neurons in the brainstem, the reticular formation. Therefore it was named the ascending reticular activating system.
They were close. In fact, the ascending pathway originates from a group of neurons around the fourth ventricle in the rostral pons (near midbrain). Most of these neurons are acetylcholinergic, and project to the thalamus, controlling whether the gate is open or closed. The key is in the action of acetylcholine. Acetylcholine cannot, by itself, activate or shut down the neurons of the thalamus. Instead it sensitizes them. By slightly depolarizing the thalamic neurons (it does this by closing a hyperpolarizing potassium channel), the ascending system can make the thalamus more sensitive to sensory input. This situation would correspond to an awake, alert state. Let's look at the whole system:

The acetylcholinergic neurons project both to the sensory areas of thalamus (such as VPL) and to the reticular nucleus, a layer of cells that wraps around the thalamus like the rind of an orange. This "reticular" has nothing to do with the "reticular" in the brainstem! The fact that the ascending reticular activating system targets the reticular nucleus is only maddening coincidence. The reticular nucleus of the thalamus has a general inhibitory effect on sensory thalamus. Now, although both areas are receiving acetylcholine, they have different receptors and respond in different ways. Sensory thalamus is sensitized by acetylcholine (or "facilitated") as described above, but the reticular nucleus is inhibited by acetylcholine. We can redraw the situation like this:

So what happens when the brain is awake? The cholinergic cells are active, so they facilitate sensory thalamus and inhibit the reticular nucleus. The inhibition of the reticular nucleus actually excites the sensory thalamus as well (negative x negative = positive). As a result the thalamus lets all sensory information through, and cortex is highly active and desynchronized dealing with all the input.
And when the brain is asleep? Now the ascending system is quiet, so sensory thalamus is not particularly sensitive. In addition, the reticular nucleus is freed from inhibition, so it can inhibit the sensory thalamus. The net effect is that thalamus is very insensitive to sensory stimuli, the gate is closed, and the cortex can rest. An interesting property of the thalamic neurons is that when hyperpolarized, they have slow intrinsic waves of activity, similar to the pacemaker of the heart. This activity may be the source of the slow synchronous pattern of the sleeping EEG. It also may function to keep the cortex in shape, ensuring that even when you are asleep the cortical neurons are active.
Summary:
Awake:
ACh system active
Sensory thalamus facilitated
Reticular nucleus inhibited
Thalamocortical neurons active
EEG desynchronous
Asleep:
ACh system inactive
Sensory thalamus inhibited
Reticular nucleus active
Thalamocortical neurons in slow rhythm
EEG synchronous
(Thanks to University of Washington for info)
I hope this has been enlightening.
~
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