As one who is involved in Forestry , it is quite obvious that the 1st paper is about the effect of dosing trees with Pramipexole and the effect this has on their final size.
The 2nd paper is concerned with the propagation of tree seeds by passing them through animals(- a bit like that coffee that goes through wild cats??)
The 3rd paper measures the final crop -preharvest - as long as it stays in the one place.
I may grasp the meaning when I read the paper completely and carefully. But I don't have the time in the next few days.
If you really want to know, pm to remind me again next week or so.
Or maybe what's his name - the guy from Oz.... aha DocUndy! He may know or find out relatively easily. He is trained as a neurologist.
At least I know that the Substantia nigra is a part deep in the brain where the high amount of dopamine and the low amount of dopamine receptors related to RLS in patients are located. So nigral lesions is when that specific part of the brain is removed. And axons are branchlike extensions of neural cells; they can be very long.
Terminal in these papers most likely refer to end-parts. And density to density of the DA (=dopamine) receptors I would guess, as it probably relates to RLS.
Yes, I'm guessing there's some form of building up of tree like structures of branching neurons, maybe ending at synapses with maybe dopamine receptors in them. I'm not clear of the relationship to dopamine receptor density and I'm not clear how the nigral lesions are occurring. If these tree-like structures are in fact new neurons, wouldn't that be good for Parkinson's?
Like you, I've a few other things to do, but it's very much part of the coalface I'm working on – unlike coalmining though, here one's got to put the pieces back together once dug out.
I have brain lesions too, all on the left side. As far as these papers go, will take some concentration, and today is not the day for that!
If it's true that persons with RLS have genetically bad dopamine transport machinery then the articles you posted, though not directly related to RLS, offer a glimmer of hope for improving (albeit likely temporarily) that dopamine transport system via dopamine antagonists. All three articles report an increase in the number and density of neurons in the striatum through the use of heavy duty dopamine antagonists. I'm guessing that even milder dopamine antagonists (like all the over the counter drugs we are supposed to avoid) might do the trick as well. By default it sounds like dopamine agonists should be avoided because they compound the problem of our genetically bad dopamine transport system. The second article indicates that unfortunately the dopamine antagonists do not have this neuron "sprouting" ability in people with lesions in that region.
To be more comprehensive, dopamine "antagonists" result in the "sprouting" of DA neurons while dopamine "agonists" result in the "pruning" of the DA neurons. Sprouting is what people with RLS want. If I was younger and in better health I would ask my naturopath if there's such a thing as an all natural dopamine antagonist with a very short half life and I would take it in the morning for a few months to see if there's any improvement. It would be great because then maybe I could stop the iron.
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Iron metabolism in RLS : iron transporter ferroportin & Magnesium Malate 
