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Dopamine and retinal function http://www.springerl...2806m205730464/

Abstract: "This review summarizes the experimental evidence in support of dopamine's role as a chemical messenger for light adaptation. Dopamine is released by a unique set of amacrine cells and activates D1 and D2 dopamine receptors distributed throughout the retina. Multiple dopamine-dependent physiological mechanisms result in an increased signal flow through cone circuits and a diminution of signal flow through rod circuits. Dopamine also has multiple trophic roles in retinal function related to circadian rhythmicity, cell survival and eye growth. In a reciprocal way, the health of the dopaminergic neurons depends on their receiving light-driven synaptic inputs. Dopamine neurons appear early in development, become functional in advance of the animal's onset of vision and begin to die in aging animals. Some diseases affecting photoreceptor function also diminish day/night differences in dopamine release and turnover. A reduction in retinal dopamine, as occurs in Parkinsonian patients, results in reduced visual contrast sensitivity"

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Adaption and Afterimages

'Adaption' means adjusting to changes in light levels http://en.wikipedia....Adaptation_(eye)

Note in the above quote, "Multiple dopamine-dependent physiological mechanisms result in an increased signal flow through cone circuits and a diminution of signal flow through rod circuits". This is refering to 'horizontal cells' in the retina which are dopaminergic (see image below).


Problems with afterimages is common among HPPD sufferes. Since some afterimaging is normal, why do HPPDers have more?

So how much is normal? It depends on changes in light levels. Normally if a person goes from sunlight to dim light it take significant time to adjust. Two main factors are 1) the time it takes for photopigments to regenerate from bleaching (what happens chemically to a rod or cone when photons strike); and 2) adjustment of the above mentioned horizontal cells (including any switching from rod vision to cone vision or back).

Complete regeneration takes 45 minutes !!! [ Trivia time: pilots preparing for night bombing missions would be put in the dark for 45 min before leaving. Later they realized that since rods are primarily responsive to green light, they could just wear dark red glasses for 45 minutes ]

For HPPDers, the second mechanism is probably the most involved. And would explain why blinking extends the time of negative afterimages. And why Sinemet can help negative afterimages.

Image 'Compression' - no one actually sees like a picture

There are 120-125 million rods in the eye. Rods are very sensitive and can respond to a single photon. But they have pigmentation that responds strongest to green so don't yield color information.

There are 5-6 million cones in the retina, centrally located. They require better than 100 photons to trigger. But they are 'color coordinated' so yield color information.

Yet there are only about 1.5 million axons (optic nerve) going to the brain. So all the signals from 125+ million photoreceptors has to be prioritized and sent to the brain. Priority is assigned by change (phasic) and 'decisions' are made by the horizontal cells (etc). If they don't have enough dopamine to respond - poor contrast and poor adaptation. Also, sympathetic states (alertness) bias reporting peripheral (rod) info. Parasympathetic states (calm) bias centeral (cone) info.

[ I am very uncertain about positive afterimaging. What I've experienced seems more in the prefrontal cortex than the eye ]

In essence, the eye doesn't see in pictures. It sees in parts broken up by changes in contrast then sent in compressed form by pulses (all neurons 'pulse'). The brain analyzes the data, assigns 'recognition' of parts based on memory of all of life's experiences, and constructs a vast network of 'precepts' that sew together into the nice stable picture of our consciousness. With HPPD, some of these processes don't work efficiently so we get all the weird stuff we think we see.

[ Examples to be added here later ]

Some homework -- http://www.cns.nyu.e...ight-adapt.html

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  • 2 weeks later...

Realy good post visual.

Im trying to get my head around it all and i have a question.(It may very well be a dumb one,sorry in advance if thats the case)

If all Sinmet does is provide more raw material to make dopemine out of, does this mean that in hppd it is the mechanism that produces the raw material for dopamine that is faulty and not the dopamine receptors themselves?



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  • 11 months later...
  • 2 weeks later...

Interesting.. I've tried both Choline Bitartrate and Alpha GPC, but never CDP-Choline.. Perhaps I'll give it a shot one of these days, if I can find a deal on ebay.

According to this, what happens is the electronic signals get bottlenecked into the Visual Cortex, am I right?
It would make sense, that with heightened excitability along those pathways, the signals get scrambled.

Also regarding dopamine: perhaps it is a localized dysfunction of tyrosine hydroxylase? It is well known for dopamine depletion to hinder vision. The only problem would be that, by following this theory, one makes the presumption that something is wrong in the retina, and not the brain. If it was merely a retinal problem, I doubt all co-morbid problems would be so prevelant.


An analysis of the distribution of dopaminergic fibres in relation to the known connections and possible functions of the deep laminae of visual cortex suggests that dopaminergic axons may participate in the corticofugal control of visual afferent pathways.



Perhaps that's more where dopamine's role comes into play. If Tyrosine Hydroxylase is deficient in that area, it would be logical for Sinemet to ameliorate visual symptoms no?

Either way, basically what you are trying to figure out is why the hell Sinemet helps HPPD symptoms, correct? Tricky stuff, I wouldn't have the darnest clue.
Good post though :)

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According to this, what happens is the electronic signals get bottlenecked into the Visual Cortex, am I right?

There are three known things that can cause these behaviours: 1) too much 'input', 2) distorted 'input', 3) too little 'input'.  Suggested reading: Hallucinations, Oliver Sacks.


Either way, basically what you are trying to figure out is why the hell Sinemet helps HPPD symptoms, correct?


Yes, accurate knowledge would be helpful here :D


We know that HPPD is a complex disorder.  That is, neural systems no longer 'balance' correctly.


Initially, it was [is] defined as damage to inhibitory serotonin receptors as can be caused by LSD.  “disinhibition of visual processing related to a loss of serotonin receptors on inhibitory interneurons,” says Henry Abraham http://dana.org/news/features/detail.aspx?id=42642


But more must be involved.  Otherwise why would Dr A look at dopamine?  The numbers show a couple genetic areas - "there was a peak at around 10 trips, and then there was another peak at around 50 trips".  Also, he observed that people with COMT polymorphisms have disinhibition problems in the frontal cortex due to 'rarification' of dopamine.  There are 2 morphisms, each with their own level of 'severity' of effect.  So he came up with the drug trial and got ~30% strong positive response.


Perhaps Klonopin works by being a substitute for this lack of inhibition.  As such, it never 'cures' because it compensates in a round about way rather than 'fixes' the damaged synapsis.  Thus people's HPPD symptoms return when discontinuing Klonopin.  It is a 'management' med.


Perhaps this too is what happens with Sinemet + tolcapone.  Members who have reported results say it worked for a couple hours up to a couple days - consistant with COMT polymorphisms and consistant with 'substituting' (though not 'proof').  So far, I am the only member reporting lasting benefits when discontinuing Sinemet, but I also use extensive 'alternative' theropies, and ... you can count on your fingers the number of people trying Sinemet (and plenty of them get the wrong formula).



So in summary, IMO, since dopaminergic synpasis are more easily damaged than other synapsis (because of dopamine processing being particularly oxidative), these are also damaged in some HPPD people.  So some symptoms relate to dopamine problems.  There is good (possible) evidence for this.


Certain HPPD symptoms match what occurs in the retina, namely sharpness, contrast and negative afterimaging.  Any weakness/distortion here would be so slight as not to be measurable by any medical equipment ... yet strong enough to cause very noticeable effects.  Certainly positive afterimages, frames, and trails are not retinal in origin since these involve memory 'gating'.  But there could be combinations such as negative afterimaging being 'amplified' by gating issues.  Again systems (plural) are involved...


In the end, 'fixing' will be the bodies own ability to grow new synapsis and/or form cortical loops.  What we can do is make the environment for healing as positive as possible - just like using a crutch for a broken leg.

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  • 3 weeks later...

Hey Visual,
sorry for never replying to your post. Anyways, I came across the following when doing searches on Choline:

Compared to vehicle-treated controls, citicoline-treated animals displayed a significantly higher retinal dopamine concentration and a tendency toward an increase in adrenaline concentration, while the noradrenaline concentration remained unchanged. It is, therefore, conceivable that citicoline reinforces dopaminergic transmission in the retina.


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