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The three neurotransmitters most central to cognition are ostensibly dopamine, glutamate, and acetylcholine.
On the other hand, we also have serotonin and gamma‑aminobutyric acid (GABA)…
Studies consistently show that those two neurotransmitters consistently lower human test scores and maze learning in rats.
“The central role of dopaminergic neurotransmission in cognitive tasks calling for working memory and executive functions is beyond dispute.”
Histamine, epinephrine, and the endorphins are important in many ways.
But they are more peripheral… They occupy more specific niches in how they shape the mind.
Dopamine is perhaps the most misunderstood neurotransmitter of them all…
And this is primarily because of just one drug: cocaine.
Cocaine is popularly known for its ability to release dopamine, the neurotransmitter falsely assumed to underlie its pleasant impact.
This is guilt by association, a presumptive practice that doesn’t always holds true.
Newer studies have shown that dopamine does not equal pleasure (hedonic principle)…
And these studies show that its role in addiction is to encode the brain to obtain more – a form of operational learning.
“Heightened dopamine neurotransmission thus appears to enhance subjective wanting, but not subjective liking, for drugs such as cocaine.”
Dopamine does this by strengthening the nerve tracts most active during the dopamine release – through D1 receptors and cAMP – thereby prioritizing the same activities the user is engaged in.
Instead, cocaine’s pleasurable effects likely derive from its activity on sigma receptors.
Historically, sigma receptors were considered a subtype of opiate receptors…
But they are now excluded from that classification because they don’t bind endogenous endorphins (i.e. enkephalins, beta‑endorphin, dynorphin).
It has since come to light that early animal food-incentive trials confounded “wanting” and “liking” – assuming that whatever is “wanted” is necessarily “liked.”
This has caused a good deal of confusion and is actually not always true…
This is evidenced by dopamine‑depleted rats “liking” things despite not actively “seeking” them.
“Conversely, dopamine agonists do not increase hedonic reactions to tastes, although they can alter their incentive value…”
Rather, we need dopamine to encode what’s worth seeking – a concept that researchers call “incentive salience.”
Dopamine also discriminates novel information from the habitual in the hippocampus by strengthening select nerve traces and depressing others.
In a similar way, dopamine also filters out noise in the frontal cortex.
And this is how it sharpens neural signals and facilitates concentration.
In all cases, dopamine discriminates between incoming sensory information, thoughts, or actions.
Dopamine is responsible for cognitive processes that shape ambition, dexterity, and adaptability.
We also need it to encode motor memory. So it should lower the learning curve in all manual tasks from typing to tennis.
And it maintains working memory in the striatum, a brain region where it exists in particularly high concentration.
“It corresponds roughly to ‘decision utility’, as that term is used in discussions of choice theory … Decision utility refers to the degree to which a goal is chosen or sought.”
Another myth surrounding dopamine is that its deficiency leads to the exaggerated shaking observed in Parkinson’s patients.
That shaking has, in fact, very little to do with dopamine itself.
It is instead caused by a minor metabolite called 3‑methoxytyramine that builds up with chronic mega-dosing of L-dopa (~5 grams per day).
Such large amounts of L-dopa are only needed to replace dopamine in fully‑depleted Parkinson’s subjects…
Average people should require much less.
Also, the universal practice of administering carbopa to Parkinson’s patients – to inhibit peripheral L-dopa metabolism – leads to far greater 3‑methoxytyramine levels…
Because more is available for methylation.
The metabolite 3‑methoxytyramine is synonymous with 3‑methyldopamine, a product of catechol‑O‑methyltransferase.
This enzyme is consistently linked to intelligence and shows great personal variation in activity.
Methoxytyramine is simply methylated dopamine, but something you don’t really want.
On average, people with the high‑activity isoforms of the enzyme have slightly lower IQs than those with the low‑activity isoforms.
We can explain this observation, generally, through dopamine inactivation.
Not surprisingly, people with the medium‑activity form generally have intermediate intelligence.
So dopamine in not our endogenous “feel-good molecule” – nor is it strictly required for movement.
Dopamine-depleted rats don’t display “shaking” – but they do lack the ambition to do much of anything.
“In other words, an accumbens opioid neural circuit is involved in hedonic activation or ‘liking.’”
Acetylcholine is the true “movement molecule” – although dopamine does play a supporting role.
Having too much acetylcholine can induce paralysis, as in organophosphate poisoning. And so can having too little.
Myasthenia gravis is a form of paralysis caused by autoantibodies that bind acetylcholine receptors.
So we’ve dispelled some myths surrounding dopamine and can see it for what it is (a cognitive enhancer)…
Now we can find the best way to upregulate its presence in the brain.
Certain ergot alkaloids – e.g. pergolide and bromocriptine – do act on dopamine receptors…
But they often interact with serotonin receptors as well and are not entirely without side effects.
Yet dopamine has a direct precursor called dihydroxy-L-phenylalanine (L-dopa).
And that has a precursor called L-tyrosine.
Both of these amino acids will act to raise brain dopamine, yet L-dopa is considerably more potent at doing so.
This is the most natural way to go about things as it doesn’t override our body’s natural control mechanisms.
“In some cases, dopamine neurons may even be more active when an animal ‘wants’ a drug reward than when it receives and presumably ‘likes’ it.”
All non‑dopamine agonists of dopamine receptors, synthetic or otherwise, activate neurons in a nonspecific manner wherever they distribute.
The amino acid L-dopa, on the other hand, is inactive as such – yet it will become dopamine to be released in discrete locations as needed.
Yet the precise dose of L-dopa matters a good deal because dopamine is known for displaying an inverted U‑shaped concentration curve.
Having too much brain dopamine – OR too little – consistently inhibits concentration and learning throughout scores of scientific trials.
While all neurotransmitters display an inverted U‑shaped curve, dopamine is characterized by perhaps the tightest one – it has the narrowest “sweet spot.”
Yet the proper dose can be figured out from the multitude of human trials invariably showing L-dopa to a beneficial effect on learning and cognition:
This was a double‑blind, placebo‑controlled study.
They used 40 male German subjects, cognitive tests, and pills containing 100 mg of L-dopa.
The participants had to learn, retain, and subsequently recall an artificial vocabulary of pronounceable German pseudo-words.
These were nonsense Lewis Carroll‑type words made even more ridiculous by having ümlauts.
It turned out, not surprisingly, that the subjects randomly assigned to the L-dopa group had better retention and recall…
That is, they could remember the meaning given to artificial words such as löek better than the non-L-dopa controls.
Moreover, a subgroup of participants with low body weight did even better.
This implies that the 100 mg dose is a bit low for your average German (82.4 kg).
There was no indication that they attained the tip of the U‑shaped curve with the 100 mg dose because beneficial results accrued linearly as a function of body weight.
“In our study, the correlation of learning success with relative dose of L-dopa (based on differences in body weight) showed not a U-shaped but a linear relation.”
This strongly implies that the most effective amount is somewhat greater than 100 mg, a dose which nonetheless has become the norm due to multiple reports of its success.
Yet the most effective dose of L-dopa is actually likely to be much greater than 100 mg, as every modern learning trial had also included 25 mg of carbidopa.
Carbidopa is an inhibitor of aromatic amino acid decarboxylase, the enzyme responsible for metabolizing L-dopa peripherally.
Using carbidopa helps to retain L-dopa plasma levels thereby allowing more to enter the brain.
Exactly to what degree it spares L-dopa is hard to determine…
That’s because all the pharmacokinetic studies had used massive doses of carbidopa and only tiny tracer‑sized amounts of [18F]-L-dopa.
Using such small amounts of [18F]-L-dopa is common because it is radioactive, thus being quite expensive and potentially dangerous.
“The L-dopa group scored better than the placebo group in this task as well. The superiority of the L-dopa group was maintained at reassessments after 1 week and 1 month.”
For this reason, it’s quite difficult (if not completely futile) to extrapolate the proper dose of L-dopa from such radically different concentrations and across species.
More reliable is perhaps to examine the studies conducted in the pre‑carbidopa era, essentially the only time when L-dopa was given “neat”:
Up to this point there were reports of L-dopa improving maze‑running in rats and also cognitive test scores in Parkinson’s patients…
Yet no studies before this had tested more‑or‑less “normal” subjects.
So these researchers used 15 of their patients in two groups…
They gave eight of them L-dopa and seven of them alpha‑methyltyrosine (a tyrosine hydroxylase inhibitor).
This was a double‑blind trial – nobody but the pharmacologist knew which participant got what until later.
The subjects served as their own controls – the researchers compared the tests scores noted under the L-dopa phase to their pre‑ and post‑trial scores.
They used rather large doses, ranging between 3 and 11 gm per day.
No data had previously been reported that would indicate the ideal dose…
Yet the large variation is suggestive of having been individually tailored for effect.
For this reason, it could be fair to assume the experimenters decided that 3–11 gm would be the “best” range.
On the other hand, 3 to 11 gm is also the range commonly used in pre‑carbidopa Parkinson’s therapy, subjects with near‑complete dopamine depletion…
So it can also be argued that it would be somewhat excessive for normal people.
Nonetheless, these substantial doses improved test scores in all subjects:
Besides body weight playing a role in individual variation, vitamin C intake should also have an effect.
This is the cofactor needed for tyrosine hydroxylase, the enzyme responsible for converting L-tyrosine into dopamine.
Well at least in vitro studies using neuroblastoma cells show that vitamin C enhances the synthesis of L-dopa.
“…a three-fold increase of tyrosine hydroxylase gene expression after five days of incubation with ascorbic acid (200 mM)…the data give evidence that ascorbic acid leads to enhanced DOPA production…by two different mechanisms… We suppose that enhancement of DOPA synthesis by ascorbic acid may be useful in the treatment of early Parkinson’s disease.”
And adding another twist in variations of L-dopa metabolism is genetic variability…
Multiple receptor and enzyme isoforms are associated with reduced or enhanced dopaminergic activity.
This study below examined five such genetic polymorphisms previously shown to affect dopamine signaling:
They used 50 participants of both sexes with an average age of 20.6 years.
The researchers drew their blood and applied PCR to determine which of the specific isoforms of each of the five important dopamine‑related proteins they expressed.
Then they tallied each subject’s number of receptors, enzymes, and transporters having high activity to obtain a combined “dopamine gene score”…
They used this score to compare against test results.
“Dopamine is a neurotransmitter that has a key role in numerous brain processes including movement, reward, learning, and plasticity.”
The learning test was a manual task involving navigating a marble through a 3 X 3 grid of nine holes with the ultimate goal of depositing the marble in the proper one.
Both the board and marble were metal.
The puzzle was constructed such that when the marble landed in the right hole, an electrical circuit closed to recorded precise completion times.
It also sounded a buzzer.
They mapped the only muscle the subjects could constructively use for the task: the first dorsal interosseous muscle of the right hand.
They did this by delivering a magnetic pulse through the subjects skulls’ around the area that usually controls the muscle.
Then they placed skin markings in the precise locations shown to activate it.
In this manner, they could remap the muscle stimulatory field as learning progressed.
This rate of change in the neuronal mapfield is considered a parameter of “brain plasticity” to be compared against the “gene score” and individual response to L-dopa.
“Thus during the placebo week, higher gene scores were associated with greater skilled motor learning. For every one point increase in gene score, the expected time to completion declined by 11.5 seconds, indicating better learning.”
They found that the subjects’ cumulative “gene score” was highly associated with learning efficiency – almost a straight line:
The “gene score” was also associated with the subjects’ response to L-dopa…
This amino acid served to benefit people naturally low on the scale and was an impediment to those naturally high on the scale.
And for that reason, the results of this study can be added to the multitude of studies revealing dopamine’s U‑shaped curve:
The subjects genetically low in dopamine activity learned better with L-dopa than without…
And those naturally high in dopamine activity became impaired by the same dose.
“The current results are congruent with this inverted U-shaped curve. On the one end of this curve, learning improved when L-dopa was given to individuals with low gene scores (with low endogenous dopamine neurotransmission)… These subjects were moved towards the optimal point. However, learning was impeded when L-dopa was given to individuals with high gene scores (with high endogenous dopamine neurotransmission)…”
So if you happen to be an impulsive person, you may want to take L-dopa a bit cautiously…
Proceed slowly while remaining cognizant of any untoward increases in compulsive behavior.
But regardless, L-dopa certainly seems to improve cognition and dexterity in more people than not…
For that reason, it can be generally framed in a good light.
Yet, on account of the substantial genetic variation which determines basal dopamine signaling, caution is always warranted with L-dopa.
Especially people with certain personality traits.
While not physically dangerous in any way, having too much dopamine can impair cognition just as well as having too little.
“Results also support the second hypothesis, with the main effect of the drug being significant…indicating that overall L-dopa improved learning…”
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- Murphy, Dennis. "Catecholamines and memory: Enhanced verbal learning during L-dopa administration." Psychopharmacologia (1972)
- Knecht, Stefan. "Levodopa: faster and better word learning in normal humans." Annals of neurology (2004)
- Pearson-Fuhrhop, Kristin. "Genetic variation in the human brain dopamine system influences motor learning and its modulation by L-Dopa." PloS one (2013)
- Cools, Roshan. "Working memory capacity predicts dopamine synthesis capacity in the human striatum." Journal of Neuroscience (2008)
- Berridge, Kent. "What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience?." Brain research reviews (1998)