I wrote: “I expect the activity in the noradrenaline brain network to change once the sleep waves change. I.e. when the sleep cycle changes so does the activity of the neuron network. I need to go look for studies that tell me wether its activity increases or decreases.
Based on my insomnia I expect it to increase. Leaving me with a surplus of noradrenaline bouncing around my head.”
But I found that noradrenaline falls before we get into REMsleep.
Prof. Mallick is very busy unraveling how noradrenaline and REMsleep are connected. He ties it to illness too. When we are REMsleep deprived, we get ill.
“My working hypothesis is that “one of the functions of REM sleep is to maintain the brain excitability (Mallick et al., 1993, 1994, 1999)” and therefore, REM sleep possibly serves house keeping function of the brain (Mallick and Singh 2011). My lab has been working towards understanding its possible cellular mechanism of action.”
This theory is very popular at the moment. Glia’s and sleep detox and stuff.
Prof. Mallick explains briefly on this page.
He links Glia-activity to Noradrenaline (NA):
“Further, the brain contains neurons as well as glia and both possess NaK ATPase. REM sleep deprivation induced increased NA stimulated neuronal NaK ATPase activity, while the glial enzyme activity was decreased. The opposite actions of NA on neuronal and glial NaK ATPase activity probably help maintain neuronal homeostasis (Baskey et al. 2009) (Fig. 4).”
(NaK ATPase is just the good old Natrium Kalium pump in every cell membrane. Sodium Potassium pump to American friends)
In his scientific research I read about the workings of glia. During sleep the cells of the brain shrink a little bit, giving room to glia and to the intercellular fluids. These two shuttle away debri and cell waste.
It is important that this all happens: the shrinking and the waste elimination.
SLEEP STAGES: REM-OFF AND REM-ON
He found that during nonREMsleep (the first five hours of my nights) there’s a continuous firing of neurons called REM-off.
Once they seize firing another set of neurons start firing, REM-on.
The REM-off/on’s activities are governed by GABA (and Noradrenaline). During REMsleep GABA is high, deactivating the Lucus Coeruleus. PubMed source here.
As long as there’s GABA, there’s REMsleep. Onset is governed by cholinergic input from the Locus Coeruleus. PubMed source here (prof. Mallick)
(cholinergic = Parasympathetic nervous system!)
REM-off neurons are called norepinephrinergic. Meaning they have to do with the SNS.
When a brain is REMsleep deprived it’s NA rises, keeping the REM-off neurons firing, prolonging the REMsleep deprivation. Gaba inhibits those pesky REM-off neurons, giving REM-on a chance. PubMed source here.
Stay away from stress, children.
During a study of blocking adrenoceptors to determine interaction between neurotransmitters and sleep this was quoted:
“Also, a critical level of norepinephrine in the system was required for the generation of REM sleep, however, a higher level may be inhibitory.”
PubMed sourcs, prod.Mallick
So you need a little bit to get to REMsleep. But too much will prevent it.
ME WANTS TO SLEEP
There must be a system governing NA levels in the brain during nonREMsleep. When it’s time to go to REMsleep the NA level will drop/rise (?) to the right level to let REMsleep commence.
In my brain the target is overshot. The NA level rises so much that I don’t get to REMsleep. I get to wake.
I think I’m onto something. I’ll investigate further. What system, what influences it?
In the mean time I’ll make sure I don’t get up while I lie awake. Getting that second stint of sleep is important. Get all the REMsleep you can.
5 hours solid sleep, 2 hours awake, 2 hours of (crappy) REMsleep. It’s the best I can do at the moment.