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Old 09-18-2008, 08:10 AM
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reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
reverett123 reverett123 is offline
In Remembrance
reverett123's Avatar
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
Default Admittedly an animal model but....

....we use them for everything else. I know this is taking place in the retina, but the optic nerve is a direct projection of the brain into space.

1: Neurochem Int. 2006 Jan;48(1):17-23. Epub 2005 Sep 26.

Diurnal patterns of dopamine release in chicken retina.

Megaw PL, Boelen MG, Morgan IG, Boelen MK.

Faculty of Science, Technology and Engineering, La Trobe University, P.O. Box 199
VIC 3552, Bendigo, Australia.

The retinal dopaminergic system appears to play a major role in the regulation of
global retinal processes related to light adaptation. Although most reports agree
that dopamine release is stimulated by light, some retinal functions that are
mediated by dopamine exhibit circadian patterns of activity, suggesting that
dopamine release may be controlled by a circadian oscillator as well as by light.
Using the accumulation of the dopamine metabolite dihydroxyphenylacetic acid
(DOPAC) in the vitreous as a measure of dopamine release rates, we have
investigated the balance between circadian- and light control over dopamine
release. In chickens held under diurnal light:dark conditions, vitreal levels of
DOPAC showed daily oscillations with the steady-state levels increasing nine-fold
during the light phase.
Kinetic analysis of this data indicates that apparent
dopamine release rates increased almost four-fold at the onset of light and then
remained continuously elevated throughout the 12h light phase.
In constant
darkness, vitreal levels of DOPAC displayed circadian oscillations, with an
almost two-fold increase in dopamine release rates coinciding with subjective
dawn/early morning. This circadian rise in vitreal DOPAC could be blocked by
intravitreal administration of melatonin (10 nmol), as predicted by the model of
the dark-light switch where a circadian fall in melatonin would relieve dopamine
release of inhibition and thus be responsible for the slight circadian increase
in dopamine release. The increase in vitreal DOPAC in response to light, however,
was only partially suppressed by melatonin. The activity of the dopaminergic
amacrine cell in the chicken retina thus appears to be dominated by
light-activated input.


PMID: 16188347 [PubMed - indexed for MEDLINE]

Or, to put it another way, when you are asleep and dawn is approaching, the (circadian) alarm clock goes off and you can stuff a (melatonin) pillow over it. But that sunlight coming in the window is far more powerful. I think that I will adjust my schedule to a morning round for now. Makes more sense from an evolutionary point too.

Somewhere in those studies above, it was noted that PWP have melatonin to dopamine ratios six times higher than normal. If that is so and morning melatonin is acting as a brake on the release of dopamine, then the more powerful light therapy could compensate, could it not?
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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