^^Good questions. OK, the function of the dopamine neurotransmitter system can manipulate both excitatory and inhibitory effects, depending on various considerations. Note for example, the typically largely sedative effects of most dopamine agonists, in the absence of some sort of broader catecholamine & adrenergic affinity that "psychostimulants" typically possess.
And dopamine is absolutely necessary for either of relaxation and deep sleep, and its scarcity causes restless leg syndrome/periodic leg movements (akathisia, I think, being an extreme case on the same spectrum) which prevent deep, restorative sleep. Dopamine agonists are the most effective treatment for this condition, and L-DOPA has also shown effectiveness. ADD patients consistently have decreased sleep quality also, and ADD has a very high comorbidity rate with RLS -- the common thread, of impaired dopaminergic transmission, is no token. And a stable regimen of therapeutic stimulant treatment for ADD tends to IMPROVE sleep quality, if the dose is not too high i.e. causing insomnia. In Parkinson's disease too, sleep quality is typically highly compromised and either of dopamine agonists or L-DOPA tend to restore it, which is rather important considering the propensity to neurotoxicity that occurs when sleep is compromised.
A lot of bodybuilders have taken to eating L-DOPA preparations before sleep, because the drug increases growth hormone and in theory this will improve body composition. Deep, restorative sleep is also necessary to growth hormone release.
The amphetamine withdrawal state, I believe, especially for people who at baseline show the symptoms of AD(H)D (hence taking amphetamine as medication), is a condition of retarded dopamine transmission. In my personal experience, I can't do much of anything BUT sleep for the first three days after I withdraw, but afterwards for about two weeks there is a tendency to insomnia. So the idea is that a dopaminergic without much concomitant adrenergic stimulation could help with this. I don't think L-DOPA will improve sleep in everyone, though. I also personally would prefer Mucuna to L-DOPA, especially unstandardized, because the duration of effect seems longer (more suited to an 8-hour sleep period, even), and for a number of reasons I suspect that the active dopaminergic fraction that helped Parkinson's patients in clinical trials (and in traditional use) is not actually L-DOPA, but perhaps another agent in combination with it. Some people are concerned about L-DOPA neurotoxicity, although I'm not so sure about it.
**(one strong theory regarding this points to the sometimes (i.e. in some areas of the brain) antagonistic relationship between acetycholine and dopamine transmission, and the disinhibition of acetylcholine that occurs when dopamine-producing cells have been killed off. Hence, you get symptoms related to cholinergic excess -- for example extreme muscle tension, and very disrupted sleep.)
edit: That was kind of an info dump, but I can provide some citations and reading if you just ask.
Edited by graatch, 06 October 2008 - 12:38 AM.