Using Dopamine Supplements to Hack Motivation: the Neurobiology of Ambition

Dopamine is the neurotransmitter that seems to make life itself rewarding. In this post, I'll teach you how to fuel your brain with dopamine supplements.

Dopamine is the motivation molecule. It makes your favorite activities exhilarating and life accomplishments satisfying. Optimizing the dopaminergic system will improve your executive function and motivation.

On the flip side: lethargy, ADHD, apathy, depression – these mental states are associated with impaired dopaminergic functioning.

If you're anything like me, then your motivation and ambition wax and wane. This can be hugely problematic if you're in the middle of a major project and need focus and energy to see it through. Nootropics and supplements are a great way to buffer your motivational reserves.

Dopamine Supplements on Amazon

I've been asked how I would spend $50 on Amazon for nootropics that support dopamine function.

Here's how you can get the most bang for your buck. If you're exclusively purchasing from Amazon, I recommend L-tyrosine, CDP-choline, and magnolia extract. Keep in mind that I go into greater detail for each of these supplements in the next section.

1. L-Tyrosine

L-tyrosine is an indirect dopamine precursor. Purchasing l-tyrosine bulk powder is a more economical way to go but can be less convenient.

First, l-tyrosine is converted to L-DOPA by tyrosine hydroxylase. Next, L-DOPA is converted to dopamine.

l-tyrosine dopamine supplement

You’re probably wondering: why not cut to the chase and take L-DOPA instead? L-DOPA is a prescription drug used to treat Parkinson’s disease and is considerably more potent than L-tyrosine (which is just an amino acid). But L-DOPA can also be neurotoxic under certain circumstances, and so I’d avoid it unless you have Parkinson’s disease.

Since l-tyrosine is a common amino acid, it’s a much gentler and healthier way to increase dopamine

2. CDP-Choline

CDP-Choline is converted to choline and uridine in vivo (in the body).

Hence, CDP-choline is traditionally grouped with cholinergic rather than dopaminergic supplements.

But researchers have also noted that CDP-choline has dopaminergic effects. It may up regulate dopamine receptor density, for example. This mechanism is advantageous because if you flood the synapse with dopamine, receptors start to downregulate. So increasing dopamine receptor density is a sustainable way to boost dopamine function.

3. Magnolia Extract

This is a traditional Chinese medicine that’s recognized for its relaxing and neuroprotective properties. It’s used to treat depression, anxiety and has mild sedative effects.

dopamine supplements magnolia

Magnolia extract is also a dopamine re-uptake inhibitor and a D5 receptor antagonist.

It may prevent 6-hydroxydopamine (6-OHDA) related lesioning of the dopamine system. 6-OHDA is an endogenous neurotoxin – meaning that it’s naturally created in your body.

See this relevant study about magnolia extract:

Interactions were demonstrated with the adenosine A(1) receptor, dopamine transporter and dopamine D(5) receptor (antagonist activity), serotonin receptors (5-HT(1B) and 5-HT(6) antagonist activity) and the GABA benzodiazepine receptor at a concentration of 100 microg/ml or lower. ME had an affinity with adenosine A(1) (K(i) of 9.2+/-1.1 microg/ml) and potentiated the GABA activated chloride current at the benzodiazepine subunits of the GABA receptor (maximum effect at 50 microg/ml). ME had a modest antagonist action with 5-HT(6) and ZE with the 5-HT(1B) receptor.

The Dark Side of Dopamine

The mechanism of action of amphetamine (Source CNS Forum)

The mechanism of action of amphetamine (Source: CNS Forum).

But before I launch into a discussion of the best dopamine supplements – I want to address the dark side of dopamine: its role in addiction, schizophrenia, and other mental illnesses.

Releasing dopamine in spades into chemical synapses in your brain doesn’t work; it’s not sustainable.

Invariably, your brain adapts to the increase and changes the homeostatic set point. A “new normal” is eventually established. This is the same mechanism underlying tolerance to drugs (tachyphylaxis).

But a gradual, gentle increase in dopamine can be beneficial. Dopamine function naturally declines with aging, and peaks in adolescence. It’s in our interests to prevent this decline to help sustain goal-oriented behavior. One way to accomplish this goal is with drugs and supplements.

Hyperdopaminergic individuals – people with naturally enhanced dopamine function – tend to be more successful because they’re more motivated, organized, and have better executive function.

But too much dopamine is linked to schizophrenia, although this link is not as cut-and-dry as previously thought. Impaired glutamate receptor function probably plays a greater role, and schizophrenics have poor executive function, suggesting dopamine hypofunction in the prefrontal cortex. A few studies have actually shown that giving stimulants to patients with schizophrenia may actually ameliorate some of their executive dysfunction.

Since we don’t want to flood chemical synapses with dopamine, it’s best to avoid psychostimulants like Adderall. Unless you have ADHD – in which case it’s beneficial but possibly neurotoxic at high doses.

Dopamine Supplements: The Complete List

Rasagiline and Selegiline

These are reasonably selective monoamine oxidase B (MAO-B) inhibitors. Since MAO-B breaks dopamine down, inhibiting this enzyme increases dopamine. These drugs were developed in Israel and are used clinically to treat Parkinson’s disease and off-label for depression.

What’s the difference between rasagiline and selegiline?

L-methamphetamine is a metabolite of selegiline, which is problematic for obvious reasons. Keep in mind that l-meth is the less active stereoisomer compared with d-meth. Rasagiline was developed as the successor to selegiline because it is cleaner, more selective and does not have any meth metabolites.

But some people respond better to selegiline and point out that l-meth may not be created in sufficient quantities to have any real adverse effects.


L-tyrosine is a common amino acid. It’s the precursor to L-DOPA, which is converted to dopamine by the enzyme AADC. The idea is that if you supplement extra l-tyrosine, this will lead to increased downstream dopamine production. This does make some sense, because tyrosine hydroxylase – the enzyme that converts tyrosine to L-DOPA is the rate-limiting step in the synthesis of dopamine. This is the bottleneck. Increase tyrosine hydroxylase activity by feeding it more l-tyrosine, and you’ll likely boost downstream dopamine.

Discussion points:
  • Since l-tyrosine is a ubiquitous amino acid, will supplementation actually have an effect?
  • Tyrosine hydroxylase is the enzyme that converts L-tyrosine to L-DOPA (the latter of which is converted to dopamine). Since Tyrosine hydroxylase is regulated by multiple mechanisms, does increasing L-tyrosine intake really translate to increased downstream dopamine production?

Apart from the above considerations, it does seem that supplemental l-tyrosine is beneficial if you’re dopamine reserves are depleted (e.g. from chronic amphetamine or cocaine use).


Nicotine is primarily a cholinergic substance. It activates nicotinic acetylcholine receptors. But it also enhances dopamine release in the mesolimbic pathway.

The smoker’s paradox is that long-term smoker’s are protected from Parkinson’s disease (though smoking is obviously unhealthy in all other respects).

One idea developed in the literature is that nicotine may protect the dopamine system. This has led to the experimental use of nicotine patches in patients with Parkinson's disease. Nicotine itself has a number of nootropic effects and is one of the few substances documented to improve working memory in healthy volunteers.


Modafinil is a pretty interesting drug. It's a wakefulness enhancer – it seems to improve vigilance and executive functioning and if you're sleep deprived and possibly even if you're well-rested.

Modafinil isn’t a potent dopamine re-uptake inhibitor like Ritalin (methylphenidate). But it does seem to be doing something to enhance dopamine function.

It has a weak affinity for the dopamine transporter, but it has many of the subjective effects linked to dopamine. The mechanism of action of modafinil isn’t fully fleshed out. It seems to affect orexin/histamine and other system that regulate wakefulness in the hypothalamus. Here's a full discussion of the mechanism of action of modafinil.

In response to inquiries about where to procure modafinil: AfinilExpress seems to be the best vendor of late.

CDP-choline / Uridine

CDP-choline is actually the precursor to both choline and uridine. Choline is acetylated to acetylcholine in vivo. Uridine is abundant in beer and other products of fermentation.

I don’t personally believe that CDP-choline is likely to have a robust effect on dopamine. But there's some promising data that’s been reported in the biomedical literature. One reason I take CDP-choline – unrelated to dopamine – is that it promotes re-myelination. The myelin sheath is what insulates axons that connect neurons. Myelinated axons can propagate a signal much faster than their exposed counterparts. That’s one reason why patients with multiple sclerosis should consider adding CDP-choline to their regimen.

CDP-choline: pharmacological and clinical review (1995):

Cytidine 5′-diphosphocholine, CDP-choline or citicoline, is an essential intermediate in the biosynthetic pathway of the structural phospholipids of cell membranes, especially in that of phosphatidylcholine. Upon oral or parenteral administration, CDP-choline releases its two principle components, cytidine and choline. When administered orally, it is absorbed almost completely, and its bioavailability is approximately the same as when administered intravenously. Once absorbed, the cytidine and choline disperse widely throughout the organism, cross the blood-brain barrier and reach the central nervous system (CNS), where they are incorporated into the phospholipid fraction of the membrane and microsomes. CDP-choline activates the biosynthesis of structural phospholipids in the neuronal membranes, increases cerebral metabolism and acts on the levels of various neurotransmitters. Thus, it has been experimentally proven that CDP-choline increases noradrenaline and dopamine levels in the CNS. Due to these pharmacological activities, CDP-choline has a neuroprotective effect in situations of hypoxia and ischemia, as well as improved learning and memory performance in animal models of brain aging.

Supplements With Dopaminergic Effects

St. John’s wort (Hypericum perforatum)

St. John’s wort is marketed as an SSRI alternative for the treatment of depression. It’s most well-recognized effects is increased serotonin by inhibiting its re-uptake; it shares this mechanism with SSRIs.

But St. John’s wort actually inhibits the re-uptake of catecholamines as well (norepinephrine and dopamine). Inhibiting re-uptake or clearance from the synapse means more neurotransmitter is left behind – so St. John’s wort augments catecholamines.

One study reported that St. John’s wort extract very preferentially inhibited dopamine uptake. The authors of the study concluded that St. John’s wort might be useful for the treatment of substance abuse. That’s because drug addiction is linked to hypoactive dopamine.

Psoralea corylifolia (Babchi)

Psoralea corylifolia (Babchi) are plants that belong to the Indian Ayurveda tradition and Chinese medical tradition.

The extract is an in vivo norepinephrine-dopamine re-uptake inhibitor (also known as an NDRI). This supplement packs a serious punch because it also preferentially inhibits monoamine oxidase B – the enzyme that breaks down catecholamines like dopamine. Other previously mentioned MAO-B inhibitors include selegiline and rasagiline.

A petroleum ether extract (FP) from Fructus Psoraleae, seeds of Psoralea corylifolia L. (Leguminosae), was found to strongly inhibit dopamine (DA) uptake by dopamine transporter (DAT) heterogeneously expressed cells (D8 cells) and noradrenaline (NE) uptake by noradrenaline transporter (NET) heterogeneously expressed cells.

For this reason, the authors indicate that biologically active compounds in Psoralea corylifolia could be used as to treat ADHD, Parkinson’s disease or cocaine addiction. These are all diseases characterized by impaired dopamine function.

However, Psoralea corylifolia may compromise our body’s defense against oxidative stress because it inhibits mitochondrial complex I. More research on this topic is needed.


Catuba literally translates to “what imparts strength to the Indian.” Like magnolia extract, it’s a bark extract, and it’s derived from trees indigenous to Brazil.

Apart from its effects on dopamine reuptake, catuba is a dopamine-releasing agent (like amphetamine). Compared with St. John’s wort, Catuba’s dopamine reuptake inhibition is more selective.

Consider this excerpt from one study1 conducted in an animal model:

In vitro, T. catigua extract concentration-dependently inhibited the uptake and increased the release of serotonin, and especially of dopamine, from rat brain synaptosomal preparations

Catuaba – A bark extract derived from several varieties of tree and often sold under the fake scientific name of Erythroxylum catuaba. Acts as a dopamine reuptake inhibitor as well as promotes the release of dopamine. Has been shown to prevent rotenone-induced apoptosis to dopamine neurons. Inhibits the reuptake of dopamine more selectively than St John’s wort.

Chinese Skullcap (Scutellaria baicalensis)

Yet another dopamine reuptake inhibitor!

Interestingly, chinese skullcap also interacts with NMDA-type glutamate receptors – specifically, the glycine binding site. Chinese skullcap’s ability to protect the brain against excitotoxicity is attributed to this mechanism.

A second study reported that chinese skullcap abolishes iron-induced dopamine neurotoxicity. Iron is an essential dietary mineral that’s necessary for hemoglobin and countless other enzymes. But it’s toxic to the central nervous system and most be sequestered by specific proteins like ferritin.

Consider this excerpt2 on the chinese skullcap/dopamine connection:

…In vitro studies showed that oroxylin A inhibited DA uptake similar to methylphenidate, a dopamine transporter blocker, but did not influence norepinephrine uptake unlike atomoxetine, a selective NE reuptake inhibitor. Collectively, the present findings suggest that oroxylin A improves ADHD-like behaviors in SHR via enhancement of DA neurotransmission and not modulation of GABA pathway as previously reported. Importantly, the present study indicates the potential therapeutic value of oroxylin A in the treatment of ADHD.

Magnolia extract (Magnolia officinalis)

This is a traditional chinese medicine that’s recognized for its relaxing and neuroprotective properties. It’s used to treat depression, anxiety, and has mild sedative effects.

What’s less well known is that magnolia extract is a dopamine reuptake inhibitor (DRI) and D5 receptor antagonist.

It may prevent 6-hydroxydopamine (6-OHDA)-induced lesioning in the brain. 6-OHDA is an endogenous neurotoxin – meaning that it’s a natural byproduct that’s formed when dopamine spontaneously auto-oxidizes.

See this relevant study about magnolia extract:

Interactions were demonstrated with the adenosine A(1) receptor, dopamine transporter and dopamine D(5) receptor (antagonist activity), serotonin receptors (5-HT(1B) and 5-HT(6) antagonist activity) and the GABA benzodiazepine receptor at a concentration of 100 microg/ml or lower. ME had an affinity with adenosine A(1) (K(i) of 9.2+/-1.1 microg/ml) and potentiated the GABA activated chloride current at the benzodiazepine subunits of the GABA receptor (maximum effect at 50 microg/ml). ME had a modest antagonist action with 5-HT(6) and ZE with the 5-HT(1B) receptor.

Jiaogulan (Gynostemma pentaphyllum)

Also referred to as jiaogulan, which literally means “typical blue plant.” It’s a climbing vine indigenous to Japan, China, Vietnam, and Korea.

Jiaogulan has antioxidant and adaptogenic properties that may enhance longevity (at least in animal models).

It also restores the dopamine system after chronic, unpredictable stress and 6-OHDA neurotoxicity (study).

Specifically, a study reported that animals treated with ethanol extracts of Gynostemma pentaphyllum 3 days after lesioning with the neurotoxin 6-OHDA markedly prevented some of the damage. In this case, Gynostemma pentaphyllum prevented the reduction in tyrosine hydroxylase (TH+) neurons that’s caused by dopaminergic neurotoxins like 6-OHDA. The authors suggest that Gynostemma pentaphyllum also resulted in no obvious signs of toxicity and were well-tolerated. This may extract may prove to be a promising prophylactic measure against Parkinson’s disease.

Bacopa (Bacopa Monnieri)

Bacopa is one of the most popular nootropics.

Researchers have reported that Bacopa blocks decrements in catecholamine levels caused by chronic stress, 6-OHDA and rotenone. On the other hand, Bacopa also blocked dopamine surges in the striatum, suggesting that it has anti-addiction properties.


N-Acetyl-Cysteine (NAC) affects the dopamine system in a manner analogous to Bacopa monnieri, albeit to a lesser extent. Consider this abstract3:

Neonatal hypoglycaemia initiates a series of events leading to neuronal death, even if glucose and glycogen stores return to normal. Disturbances in the cortical dopaminergic function affect memory and cognition. We recommend Bacopa monnieri extract or Bacoside A to treat neonatal hypoglycaemia. We investigated the alterations in dopaminergic functions by studying the Dopamine D1 and D2 receptor subtypes. Receptor-binding studies revealed a significant decrease (p < 0.001) in dopamine D1 receptor number in the hypoglycaemic condition, suggesting cognitive dysfunction. cAMP content was significantly (p < 0.001) downregulated in hypoglycaemic neonatal rats indicating the reduction in cell signalling of the dopamine D1 receptors. It is attributed to the deficits in spatial learning and memory. Hypoglycaemic neonatal rats treated with Bacopa extract alone and Bacoside A ameliorated the dopaminergic and cAMP imbalance as effectively as the glucose therapy. The upregulated Bax expression in the present study indicates the high cell death in hypoglycaemic neonatal rats. Enzyme assay of SOD confirmed cortical cell death due to free radical accumulation. The gene expression of SOD in the cortex was significantly downregulated (p < 0.001). Bacopa treatment showed a significant reversal in the altered gene expression parameters (p < 0.001) of Bax and SOD. Our results suggest that in the rat experimental model of neonatal hypoglycaemia, Bacopa extract improved alterations in D1, D2 receptor expression, cAMP signalling and cell death resulting from oxidative stress. This is an important area of study given the significant motor and cognitive impairment that may arise from neonatal hypoglycaemia if proper treatment is not implemented.


The amphetamine (AMPH)-induced alteration in rat brain dopamine levels modified by N-acetylcysteine (NAC) administration has been examined using isocratic ion-pair reversed-phase high-performance liquid chromatography with electrochemical detection. The aim of the development of a novel validated evaluation scheme implying a double AMPH challenge was to enhance the efficiency of AMPH-triggered dopamine release measurements in rat brain striatal slices by improving the reproducibility of the results. The proposed experimental protocol was tested in vivo and proved to be capable of fast and reliable drug screening for tracing the effect of NAC as a model compound in AMPH-mediated dopaminergic response. The subcellular localization of the dopamine mobilizing effect of NAC has been established indirectly by the use of an irreversible dopamine vesicular depletor, reserpine. The antioxidant NAC at 10 mM plays an important role in the complete suppression of acute AMPH-elicited dopamine release. The possible role of this quenching effect is discussed.

Alpha GPC

Alpha-GPC has been noted to increase dopamine transporter (DAT) density and potassium-stimulated dopamine release, along with raising DOPAC levels in the cerebellum as well as the frontal cortex5.

Choline-containing phospholipids were proposed as cognition enhancing agents, but evidence on their activity is controversial. CDP-choline (cytidine-5´-diphosphocholine, CDP) and choline alphoscerate (L-alpha-glycerylphosphorylcholine, GPC) represent the choline-containing phospholipids with larger clinical evidence in the treatment of sequelae of cerebrovascular accidents and of cognitive disorders. These compounds which display mainly a cholinergic profile interfere with phospholipids biosynthesis, brain metabolism and neurotransmitter systems. Dated preclinical studies and clinical evidence suggested that CDP-choline may have also a monoaminergic profile. The present study was designed to assess the influence of treatment for 7 days with choline-equivalent doses (CDP-choline: 325 mg/Kg/day; GPC: 150 mg/Kg/day) of these compounds on brain dopamine (DA), and serotonin (5-HT) levels and on DA plasma membrane transporter (DAT), vesicular monoamine transporters (VMAT1 and VMAT2), serotonin transporter (SERT), and norepinephrine transporter (NET) in the rat. Frontal cortex, striatum and cerebellum were investigated by HPLC with electrochemical detection, immunohistochemistry, Western blot analysis and ELISA techniques. CDP-choline did not affect DA levels, which increased after GPC administration in frontal cortex and cerebellum. GPC increased also 5-HT levels in frontal cortex and striatum. DAT was stimulated in frontal cortex and cerebellum by both CDP and GPC, whereas VMAT2, SERT, NET were unaffected. VMAT1 was not detectable. The above data indicate that CDP-choline and GPC possess a monoaminergic profile and interfere to some extent with brain monoamine transporters. This activity on a relevant drug target, good tolerability and safety of CDP-choline and GPC suggests that these compounds may merit further investigations in appropriate clinical settings.

Gingko Biloba

A MAO-B inhibitor that appears to preferentially elevate noradrenaline and dopamine over other monoamines.

Jatamansi (Nardostachys jatamansi)6 is another MAO-B inhibitor that seems to preferentially increase 5HT and GABA so than adrenaline and dopamine. Additionally prevents 6-OHDA induced neurodegeneration of dopaminergic systems.

The effect of acute and subchronic administration of an alcoholic extract of the roots of Nardostachys jatamansi on norepinephrine (NE), dopamine (DA), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), gamma-aminobutyric acid (GABA), and taurine were studied in male albino Wistar rats. The acute oral administration of the extract did not change the level of NE and DA but resulted in a significant increase in the level of 5-HT and 5-HIAA. A significant increase in the level of GABA and taurine was observed in the drug-treated groups when compared to the controls. A 15-day treatment resulted in a significant increase in the levels of NE, DA, 5-HT, 5-HIAA, and GABA. These data indicate that the alcoholic extract of the roots of N. jatamansi causes an overall increase in the levels of central monoamines and inhibitory amino acids.

A close cousin of clary sage, Salvia palaestina, shows promise at the same time since it’s parts which have high binding affinity with dopamine receptors at amounts that are reasonably low, yet it’s significantly understudied.

RESULTS: Among the essential oils tested, 5% (v/v) clary oil had the strongest anti-stressor effect in the FST. We further investigated the mechanism of clary oil antidepression by pretreatment with agonists or antagonists to serotonin (5-HT), dopamine (DA), adrenaline, and GABA receptors. The anti-stressor effect of clary oil was significantly blocked by pretreatment with buspirone (a 5-HT(1A) agonist), SCH-23390 (a D(1) receptor antagonist) and haloperidol (a D(2), D(3), and D(4) receptor antagonist).

CONCLUSIONS: Our findings indicate that clary oil could be developed as a therapeutic agent for patients with depression and that the antidepressant-like effect of clary oil is closely associated with modulation of the DAnergic pathway.


Beta-alanine7 enhances dopamine release in the nucleus accumbens by activating the glycine receptor.

Glycine receptors (GlyRs) in the nucleus accumbens (nAc) have recently been suggested to be involved in the reinforcing and dopamine-elevating properties of ethanol via a neuronal circuitry involving the VTA. Apart from ethanol, both glycine and taurine have the ability to modulate dopamine output via GlyRs in the same brain region. In the present study, we wanted to explore whether yet another endogenous ligand for the GlyR, beta-alanine, had similar effects. To this end, we monitored dopamine in the nAc by means of in vivo microdialysis and found that local perfusion of beta-alanine increased dopamine output. In line with previous observations investigating ethanol, glycine and taurine, the competitive GlyR antagonist strychnine completely blocked the dopamine elevation. The present results suggest that beta-alanine has the ability to modulate dopamine levels in the nAc via strychnine-sensitive GlyRs, and are consistent with previous studies suggesting the importance of this receptor for modulating dopamine output.

The Take Home Message

It’s hard to increase dopamine without homeostatic mechanisms kicking in. I’m talking about tachyphylaxis, where receptors become less sensitive in the presence of too much of a good thing (dopamine, or any ligand for that matter). But gently increasing dopamine using different strategies is a viable way to enhance motivation, concentration, and productivity.

I’ve had success using low-dose nicotine and low-dose selegiline. Modafinil less clearly affects dopamine. But it does seem to recapitulate some of the benefits of the more purely dopaminergic substances. See this list to learn about my favorite nootropics.

  1. Campos MM, Fernandes ES, Ferreira J, Santos AR, Calixto JB. Antidepressant-like effects of Trichilia catigua (Catuaba) extract: evidence for dopaminergic-mediated mechanisms. Psychopharmacology (Berl). 2005;182(1):45-53. Link to abstract

  2. Yoon SY, Dela peña I, Kim SM, et al. Oroxylin A improves attention deficit hyperactivity disorder-like behaviors in the spontaneously hypertensive rat and inhibits reuptake of dopamine in vitro. Arch Pharm Res. 2013;36(1):134-40. Link to abstract.

  3. Thomas RB, Joy S, Ajayan MS, Paulose CS. Neuroprotective potential of Bacopa monnieri and Bacoside A against dopamine receptor dysfunction in the cerebral cortex of neonatal hypoglycaemic rats. Cell Mol Neurobiol. 2013;33(8):1065-74. Link to abstract.

  4. Gere-pászti E, Jakus J. The effect of N-acetylcysteine on amphetamine-mediated dopamine release in rat brain striatal slices by ion-pair reversed-phase high performance liquid chromatography. Biomed Chromatogr. 2009;23(6):658-64. Link to abstract.

  5. Tayebati SK, Tomassoni D, Nwankwo IE, et al. Modulation of monoaminergic transporters by choline-containing phospholipids in rat brain. CNS Neurol Disord Drug Targets 2013;12(1):94-103.

  6. Seol GH, Shim HS, Kim PJ, et al. Antidepressant-like effect of Salvia sclarea is explained by modulation of dopamine activities in rats. J Ethnopharmacol. 2010;130(1):187-90.

  7. Ericson M, Clarke RB, Chau P, Adermark L, Söderpalm B. beta-Alanine elevates dopamine levels in the rat nucleus accumbens: antagonism by strychnine. Amino Acids. 2010;38(4):1051-5.

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Ben Gardner

I'm interested in nutrition, nootropics, and javascript. I'm a firm believer in getting really good at one thing.


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