Dopamine uses. Dopamine: Uses, Mechanism of Action, and Clinical Applications

22.09.202307.07.2023 by alexxlab

What are the primary uses of dopamine in clinical settings. How does dopamine work at different infusion rates. What are the key indications for dopamine therapy. How is dopamine synthesized in the body. What are the main dopamine receptor families and their effects.

Содержание

Understanding Dopamine: A Crucial Neurotransmitter and Medication

Dopamine is a fascinating compound that plays dual roles in the human body – as a neurotransmitter in the central nervous system and as a medication used in various clinical settings. This article delves into the complex world of dopamine, exploring its uses, mechanism of action, and clinical applications.

Clinical Uses of Dopamine: From Cardiovascular Support to Neurological Treatment

Dopamine finds extensive use in medical practice, primarily as a peripheral vasostimulant. Its applications include:

Treatment of low blood pressure
Management of low heart rate
Intervention in cardiac arrest situations
Support in acute neonatal cases

Are there different effects of dopamine at varying infusion rates? Indeed, the impact of dopamine administration depends significantly on the infusion rate:

Low infusion rates (0.5 to 2 micrograms/kg per minute): Act on visceral vasculature, producing vasodilation, especially in the kidneys, leading to increased urinary flow.
Intermediate infusion rates (2 to 10 micrograms/kg/min): Stimulate myocardial contractility and enhance electrical conductivity in the heart, resulting in increased cardiac output.
High infusion rates (above 10 micrograms/kg/min): Cause vasoconstriction and increase blood pressure via adrenergic receptors, potentially leading to poor peripheral circulation.

Indications for Dopamine Therapy: Beyond Cardiovascular Support

While dopamine is primarily known for its cardiovascular effects, its therapeutic applications extend beyond this realm. What are the key indications for dopamine therapy?

Maintenance of blood pressure in chronic congestive heart failure
Management of trauma-induced hypotension
Support in renal failure
Cardiovascular support during open-heart surgery
Management of shock from myocardial infarction or septicemia
Treatment of hypotension and low cardiac output
Improvement of inadequate organ perfusion, often indicated by low urine production

Dopamine in Neurological Disorders: The Parkinson’s Connection

Dopamine gained significant clinical importance in the central nervous system after groundbreaking experiments by Hornykiewicz. These studies revealed a reduction of dopamine within the caudate nucleus of patients with Parkinson’s disease. This discovery led to a major breakthrough in Parkinson’s treatment – the use of L-DOPA (L-dihydroxyphenylalanine), the amino acid precursor of dopamine.

Why can’t dopamine itself be used to treat Parkinson’s disease? The blood-brain barrier prohibits the crossing of dopamine from the systemic circulation into the central nervous system. Consequently, intravenous dopamine is ineffective for central neurological deficits like Parkinson’s disease. However, L-DOPA can successfully cross the blood-brain barrier and can be administered systemically, including in oral form.

Does L-DOPA treatment come with any downsides? While the therapeutic replacement of dopamine effectively alleviates motor symptoms in Parkinson’s disease, it may lead to motor side-effects and behavioral issues associated with addiction, such as impulse control disorders.

The Intricate Process of Dopamine Biosynthesis

Understanding how dopamine is synthesized in the body provides crucial insights into its function and potential therapeutic interventions. What is the process of dopamine biosynthesis?

The first step is rate-limiting and involves converting L-tyrosine to L-DOPA. This conversion is catalyzed by the enzyme tyrosine hydroxylase (TH).
The conversion requires oxygen, an iron co-factor, and tetrahydrobiopterin (Bh5 or THB).
This process results in adding a hydroxyl group to the aromatic ring of L-tyrosine, forming L-DOPA.
L-DOPA is then converted to dopamine by the enzyme aromatic L-amino acid decarboxylase, which removes the carboxyl group.
Once synthesized, dopamine is transported into synaptic vesicles via the vesicular monoamine transporter 2 (VMAT2) to the synaptic terminals.

It’s worth noting that if an individual regularly consumes L-tyrosine in abundance, it readily crosses the blood-brain barrier, as does L-DOPA. However, if L-tyrosine levels are low, L-phenylalanine may be converted into L-tyrosine by phenylalanine hydroxylase.

Dopamine Receptors: The Key to Its Diverse Effects

The diverse effects of dopamine are mediated through its interaction with various receptors. What are the main families of dopamine receptors?

There are two entire families of dopamine receptors composed of five different isoforms, each affecting different intracellular signaling pathways:

D1 receptor family
D2 receptor family

Both families of dopamine receptors are G-protein-coupled receptors. However, their effects on intracellular signaling pathways differ. The D1 receptor class activation results in increased cyclic AMP (cAMP) production, while the D2 receptor class inhibits cAMP production.

D1 Receptor Family

The D1 receptor family includes two subtypes:

D1 receptors
D5 receptors

These receptors are primarily found postsynaptically and are coupled to Gs proteins. Activation of D1-like receptors leads to increased adenylyl cyclase activity, resulting in increased cAMP production.

D2 Receptor Family

The D2 receptor family includes three subtypes:

D2 receptors
D3 receptors
D4 receptors

These receptors can be found both pre- and postsynaptically and are coupled to Gi/o proteins. Activation of D2-like receptors leads to inhibition of adenylyl cyclase, resulting in decreased cAMP production.

Dopamine’s Role in Reward and Motivation

Beyond its clinical applications, dopamine plays a crucial role in the brain’s reward system. How does dopamine contribute to reward and motivation?

Dopamine is often referred to as the “feel-good” neurotransmitter due to its role in pleasure and reward. When we experience something pleasurable, dopamine is released in certain areas of the brain, particularly the nucleus accumbens. This release of dopamine reinforces the pleasurable experience, making us more likely to repeat the behavior that led to it.

This mechanism is essential for motivation and learning. It helps us form habits and drives us to seek out rewarding experiences. However, this same system can also play a role in addiction. Drugs of abuse often hijack this reward system, leading to abnormally high levels of dopamine release and potentially addictive behavior.

Dopamine and Decision-Making

Dopamine also plays a crucial role in decision-making processes. It’s involved in:

Anticipation of reward
Risk assessment
Effort-based decision making

When we anticipate a reward, dopamine levels increase, influencing our decisions and driving us towards actions that we expect will lead to positive outcomes. This anticipatory release of dopamine is a key factor in motivation and goal-directed behavior.

Dopamine Imbalances and Associated Disorders

Given dopamine’s wide-ranging effects in the body and brain, it’s not surprising that imbalances in dopamine levels or function can lead to various disorders. What are some conditions associated with dopamine imbalances?

Parkinson’s Disease: Characterized by a loss of dopamine-producing neurons in the substantia nigra, leading to motor symptoms.
Schizophrenia: Thought to involve an overactive dopamine system in certain brain areas.
ADHD (Attention Deficit Hyperactivity Disorder): May involve dysfunctions in dopamine signaling.
Depression: Can involve reduced dopamine activity in certain brain regions.
Addiction: Involves dysregulation of the brain’s reward system, in which dopamine plays a central role.

Understanding these disorders and their relationship to dopamine has led to the development of various therapeutic approaches. For instance, L-DOPA is used to treat Parkinson’s disease, while antipsychotic medications often target dopamine receptors to manage schizophrenia symptoms.

Dopamine and Cognitive Function

Beyond its role in movement and reward, dopamine is also crucial for various cognitive functions. How does dopamine influence cognition?

Working Memory: Dopamine in the prefrontal cortex is essential for working memory function.
Attention: Dopamine plays a role in regulating attention and focus.
Cognitive Flexibility: The ability to adapt behavior in response to changing environmental demands is influenced by dopamine.
Learning: Dopamine is involved in both reinforcement learning and associative learning processes.

These cognitive functions are crucial for daily life and can be impaired in conditions involving dopamine dysfunction. This understanding has led to research into dopamine-based therapies for cognitive enhancement and the treatment of cognitive disorders.

Future Directions in Dopamine Research and Therapy

As our understanding of dopamine’s complex roles in the body and brain continues to grow, what are some promising areas for future research and therapeutic development?

Targeted Dopamine Therapies: Developing medications that can target specific dopamine receptor subtypes or act in specific brain regions could lead to more effective treatments with fewer side effects.
Gene Therapy: Research into gene therapy approaches for conditions like Parkinson’s disease, aiming to restore dopamine production in affected brain areas.
Personalized Medicine: Using genetic and neuroimaging data to tailor dopamine-based treatments to individual patients.
Novel Drug Delivery Methods: Developing new ways to deliver dopamine or dopamine agonists across the blood-brain barrier could open up new treatment possibilities.
Dopamine and Neuroplasticity: Further research into dopamine’s role in brain plasticity could lead to new approaches for neurorehabilitation and cognitive enhancement.

These areas of research hold promise for improving our ability to treat a wide range of disorders, from neurological conditions like Parkinson’s disease to psychiatric disorders and cognitive impairments.

Dopamine and Lifestyle Factors

While much focus is placed on pharmacological interventions involving dopamine, it’s also important to consider how lifestyle factors can influence dopamine function. What are some ways that lifestyle choices can impact dopamine levels and function?

Exercise: Regular physical activity has been shown to increase dopamine synthesis and release.
Diet: Certain foods, particularly those rich in tyrosine (the precursor to dopamine), may influence dopamine levels.
Sleep: Adequate sleep is crucial for maintaining healthy dopamine function.
Stress Management: Chronic stress can negatively impact dopamine signaling.
Social Interaction: Positive social experiences can boost dopamine activity.

Understanding these factors can provide additional tools for managing dopamine-related conditions and promoting overall brain health. It also underscores the importance of a holistic approach to health that considers both medical interventions and lifestyle factors.

Ethical Considerations in Dopamine Research and Therapy

As our ability to manipulate dopamine systems grows, so too do the ethical considerations surrounding this field of research and treatment. What are some key ethical issues to consider?

Enhancement vs. Treatment: Where do we draw the line between treating disorders and enhancing normal function?
Addiction Potential: How do we balance the therapeutic benefits of dopaminergic drugs with their potential for addiction?
Informed Consent: Given dopamine’s role in decision-making, how do we ensure truly informed consent in dopamine-related research?
Privacy Concerns: As we develop more sophisticated ways to measure and manipulate dopamine function, how do we protect individuals’ neurological privacy?
Equity in Access: How can we ensure that advances in dopamine-based therapies are accessible to all who need them?

These ethical considerations highlight the need for ongoing dialogue between scientists, clinicians, ethicists, policymakers, and the public as we continue to advance our understanding and manipulation of dopamine systems.

Dopamine in Popular Culture

The concept of dopamine has permeated popular culture, often in simplified or misunderstood ways. How is dopamine represented in popular media and culture?

“Dopamine Rush”: Often used to describe feelings of pleasure or excitement, though this is an oversimplification of dopamine’s role.
Addiction Narratives: Dopamine is frequently mentioned in discussions of addiction, sometimes overstating its role.
Self-Help and Productivity: Some productivity gurus promote “dopamine fasting” or other dopamine-related life hacks, often based on misunderstandings of the neuroscience.
Social Media: Discussions of social media addiction often invoke dopamine, though the reality is more complex.

While these popular representations have increased public awareness of dopamine, they often oversimplify its complex roles in the brain and body. This underscores the importance of accurate scientific communication to bridge the gap between research findings and public understanding.

As we continue to unravel the mysteries of dopamine, from its basic biochemistry to its complex roles in behavior and cognition, we open up new possibilities for understanding and treating a wide range of human conditions. The story of dopamine is far from over, and future research promises to yield even more fascinating insights and therapeutic possibilities.

Dopamine – StatPearls – NCBI Bookshelf

Continuing Education Activity

Dopamine is a peripheral vasostimulant used to treat low blood pressure, low heart rate, and cardiac arrest. Low infusion rates (0.5 to 2 micrograms/kg per minute) act on the visceral vasculature to produce vasodilation, including the kidneys, resulting in increased urinary flow. Intermediate infusion rates (from 2 to 10 micrograms/kg/min) stimulate myocardial contractility and increase electrical conductivity in the heart leading to increased cardiac output. Higher doses cause vasoconstriction and increased blood pressure via the adrenergic receptors alpha-1, beta-1, and beta-2, potentially leading to poor peripheral circulation. This activity will highlight the mechanism of action, adverse event profile, pharmacology, monitoring, and relevant interactions of doxorubicin, pertinent for members of the interprofessional team in the treatment of patients with indicated conditions.

Objectives:

Identify the mechanism of action at various doses of dopamine.
Review the indications for therapy with dopamine.
Outline the potential adverse effects of dopamine therapy.
Summarize the importance of interprofessional communication and improving care coordination among the interprofessional team when initiating dopamine therapy.

Access free multiple choice questions on this topic.

Indications

Dopamine (DA) is a peripheral vasostimulant used to treat low blood pressure, low heart rate, and cardiac arrest, especially in acute neonatal cases via a continuous intravenous drip.[1] Low infusion rates (0.5 to 2 micrograms/kg per minute) act on the visceral vasculature to produce vasodilation, including the kidneys, resulting in increased urinary flow. Intermediate infusion rates (from 2 to 10 micrograms/kg/min) stimulate myocardial contractility and increase electrical conductivity in the heart leading to increased cardiac output. Higher doses cause vasoconstriction and increased blood pressure via the adrenergic receptors alpha-1, beta-1, and beta-2, potentially leading to poor peripheral circulation. [2]

Indications for DA include maintenance of blood pressure for chronic congestive heart failure, trauma, renal failure, and even open-heart surgery and shock from myocardial infarction or septicemia. DA administration in low doses may also be beneficial to manage hypotension, low cardiac output, and inadequate organ perfusion (often indicated by low urine production). DA gained significant clinical importance in the central nervous system (CNS) after Hornykiewicz’s experiments showed its reduction within the caudate nucleus of patients with Parkinson disease. Furthermore, the intravenous administration of its amino acid precursor, L-DOPA (L–dihydroxyphenylalanine), attenuated the Parkinsonian symptoms.[3] Since the blood-brain barrier prohibits the crossing of DA into the CNS from the systemic circulation, DA is ineffective on central neurological deficits such as Parkinson disease. However, L-DOPA successfully crosses the blood-brain barrier and can be administered systemically, including oral pills. Although the therapeutic replacement of dopamine effectively alleviates motor symptoms, it may lead to motor side-effects and behavioral issues associated with addiction (i.e., impulse control disorders.)[4]

Mechanism of Action

Dopamine biosynthesis occurs following the same enzymatic sequence as norepinephrine (NE). In fact, DA is a precursor in the synthesis of NE (see Figure).[5][6] The first step of DA synthesis is rate-limiting and involves converting L-tyrosine to L-DOPA by the enzyme tyrosine hydroxylase (TH) enzyme.[7][8][9] This conversion requires oxygen, an iron co-factor, and tetrahydrobiopterin (Bh5 or THB) and results in adding a hydroxyl group to the aromatic ring to form L-DOPA. This molecule subsequently converts to DA by the aromatic L-amino acid decarboxylase, involving removing the carboxyl group. Once synthesized, DA is transported into synaptic vesicles via the vesicular monoamine transporter 2 (VMAT2) to the synaptic terminals.[10][11][12]

If an individual regularly consumes L-tyrosine in abundance, it readily crosses the blood-brain barrier, as does L-DOPA. [13]. But its utility is spatially restricted because DA cannot cross the blood-brain barrier. However, if L-tyrosine levels are low, L-phenylalanine may be converted into L-tyrosine by phenylalanine hydroxylase.

After DA release into the synaptic space, it interacts with various receptors on the pre and post-synaptic terminals, causing neuronal excitation or inhibition at the target neuron. There are two entire families of DA receptors composed of five different isoforms, each affecting different intracellular signaling pathways.[14] Both families of dopamine receptors, D1 and D2, are, by definition, G-protein-coupled receptors, but the D1 receptor class results in the neuron’s depolarization, whereas the D2 receptors inhibit neuronal firing.[15]

Once in the synaptic cleft, DA is transported back into the pre-synaptic neuron via DA transporters (DAT) for repackaging or can remain in the extracellular space to be taken up by glial cells or metabolized by the cellular membrane. DA may be metabolized extraneuronally by catechol-o-methyltransferase (COMT) to 3-methoxytyramine (3-MT), while monoamine oxidase-B (MAO-B) will rapidly metabolize 3-MT to homovanillic acid (HVA).[16][17] Alternatively, it may undergo metabolism inside the cytoplasm, where the dual action of MAO-A and aldehyde dehydrogenase (ALDH) will convert DA to the phenolic acid 3, 4-dihydroxyphenylacetic acid (DOPAC).[18]

Given this complex sequence, the modulation of dopamine can occur at various levels, such as the entire neuron, its projections, or the neuronal circuitry across the nervous system. Also, during the synthesis of DA (transcriptional, translational, and post-translational regulation), synaptosomal packaging (regulation of VMAT, transport of vesicle to synapse), DA release (neuronal depolarization, calcium signaling, vesicle fusion), and via reuptake and metabolism through regulation of the respective enzymes and their spatial localization relative to their substrate.[18][19]

As indicated earlier, the systemic action of DA is subject to mediation by various receptors (D1, D2, D3, D4, and D5) and the alpha- and beta-adrenergic receptors. These G-coupled receptors generally group as either D1 or D2, primarily based on their traditional biochemical functions showing that dopamine can modulate adenylyl cyclase activity.[6][20] However, based on their molecular structure, biochemical properties, and pharmacological functions, DA receptors are further classified either as D1-class (D1 and D5) or D2-class (D2, D3, D4).[21][22][23][15]

Activation of the D1 receptors on smooth muscle, the proximal renal tubule, and cortical collecting duct increase diuresis.[24] D2 receptors are located pre-synaptically on the renal nerves and within the glomeruli and adrenal cortex. The activation of these nerves results in decreased renal sodium and water excretion.[25] Apomorphine is a DA receptor agonist and may have similar activation on these DA receptors.[26] Adrenergic receptors also bind DA increasing arterial smooth muscle contraction and cardiac sinoatrial node conductivity, which explains its cardiac therapeutic benefits.

While the blood-brain barrier specifically restricts the transport of DA from the systemic circulation to the central nervous system, further research has led to the discovery of its central role in reward-seeking behavior, wherein its transmission becomes markedly increased. Current DA research includes epigenetic changes and their involvement in a variety of psychiatric conditions, including substance abuse and addiction, schizophrenia, and attention deficit disorder.[27][28] Altogether, these conditions involve disorders of the mesolimbic and mesocortical DA pathways. One common effect of addictive drugs in the CNS is the increased release of DA in the striatum, classically associated with high locomotor activity and stereotypy.[29][30] The striatal DA increase results from axon projections arising directly from the pars compacta of the substantia nigra (SN) and the ventral tegmental area (VTA), respectively, which project to the nucleus accumbens and amygdala, implicated in reward-stimulation and the fear-response.[29][31][32]

Another DA circuit, the tuberoinfundibular pathway, is mainly responsible for regulating the neuroendocrine prolactin from the anterior pituitary gland, known for its role as a lactation inducer, but also has lesser roles in water/salt homeostasis and immune response and cell-cycle regulation. [33][34] The nigrostriatal pathway is the main pathway involved in the motor deficits observed in Parkinson’s disease.[35] This pathway comprises dopaminergic neurons originating in the substantia nigra (pars compacta) and projects to the striatum via the medial forebrain bundle, forming synapses with several neuronal populations at the putamen, caudate nucleus, globus pallidus internus (GPi), and the subthalamic nucleus (STN), respectively. This elaborated network forms the afferent connections of the substantia nigra to the circuitry involved in motor movement, namely the basal ganglia. In the latter, DA plays a pivotal function in controlling motor movement and learning new motor skills.[36]

Administration

For stimulation of the sympathetic nervous system, the indication is for a continuous intravenous drip administration. Dopamine half-life in the systemic circulation is between 1 to 5 minutes; thus, slower forms of administration, such as oral administration, are typically ineffective. [37]

In addition to its peripheral sympathetic effects, DA is also critical for neurological movement function in Parkinson’s disease.[35] L-DOPA administration is via the oral route, and after its absorption, a small percentage transports to the brain, where the neurons use it in the basal ganglia. L-DOPA is generally administered concomitantly with carbidopa to inhibit the peripheral effects of L-DOPA in the sympathetic nervous system. Carbidopa is a decarboxylase inhibitor that prevents the systemic conversion of L-DOPA to DA, which decreases the presentation of common side effects such as nausea and emesis.[38]

Adverse Effects

Dopamine administration can adversely affect kidney function, causing increased urinary flow and irregular heartbeat.[39] Excessive administration may cause deleterious conditions such as cerebrovascular accidents due to elevated blood pressure in the brain.[40]

As previously stated, the neurotransmitter DA also acts centrally within the mesocorticolimbic pathway and has roles in processing reward and fear, as well as focusing attention and executive functioning, including complex planning. [31][32] While systemic dopamine does not cross the blood-brain barrier, central dopamine carries implications in somnolence, schizophrenia, addiction, and impulse control disorders.[13][27][41] Patients with neurologic conditions using high doses of L-DOPA for Parkinson disease may experience such physiological alterations from the dysregulation of DA within the CNS pathways.

Contraindications

In patients with conditions of the heart or circulatory system, the intravenous administration of dopamine is contraindicated. These conditions may include ventricular arrhythmias and tachycardia, blood vessel blockage, low blood-oxygen content, decreased blood volume, acidosis, and adrenal gland dysfunctions resulting in high blood pressure such as pheochromocytoma. For patients recently treated with monoamine oxidase inhibitors, DA is initially used in fractional doses (one-tenth usual dose) and closely monitored for further effects. Medications to treat hypertension, such as beta and alpha-adrenergic inhibitors, antagonize the therapeutic effects of DA. Haloperidol also blocks the systemic effects of DA. The anticonvulsant phenytoin has been reported to cause hypotension and decreased heart rate when used with DA. On the other hand, tricyclic antidepressants increase the DA response, similar to anesthetic agents such as cyclopropane and halogenated. In combination with oxytocin, the use of DA can lead to chronic hypertension and may also cause cerebrovascular accidents.[42]

Monitoring

Monitoring blood pressure and urine flow is necessary — monitoring of more advanced hemodynamic parameters such as cardiac output, including rhythm and pulmonary wedge pressure, is also recommended. It is worth noting that dopamine agonists and mimetics that cross the blood-brain barrier interact with the neurological circuitry involved in motor, executive, and limbic functions, including addiction-linked reward systems, impulse control mechanisms, and arousal. Thus, the cessation of DA therapies may lead to a condition called dopamine agonist withdrawal syndrome. This condition has wide-ranging symptoms, including anxiety, depression, panic attacks, fatigue, hypotension, nausea, irritability, and even suicidal ideations.[43] Therefore, recommendations are to taper patients off of these centrally acting DA agonists.

Toxicity

According to “Sax’s Dangerous Properties of Industrial Materials” (by Richard J. Lewis, 2004 – DOI: 10.1002/0471701343), studies in rodents showed an LD50 (a lethal dose in 50% of subjects) between 59 to 163 mg/kg. In humans, dopamine can lead to peripheral vasoconstriction resulting in gangrenous extremities and cardiac arrhythmias.[44][45]

Enhancing Healthcare Team Outcomes

Dopamine administration affects the cardiovascular system, as well as other organs, including the kidneys and the brain. Contraindications include specific pharmaceutical agents, lifestyle, and nutrition factors that can impact similar organs with DA treatment. These factors and medications include psychopharmacological agents, neuroleptics, general anesthetics, and even physical therapy-induced cardiac challenges. Communication among all interprofessional healthcare team members, including clinicians, mid-level practitioners, nurses, pharmacists, and therapists, is critical to ensuring proper application of DA to mitigate potentially harmful or chronic adverse effects while considering a holistic healthcare approach along with specific outcome objectives. By engaging in interprofessional teamwork and communication, dopamine therapy can achieve its best possible outcomes with the fewest adverse events. [Level 5]

Review Questions

Access free multiple choice questions on this topic.
Comment on this article.

Figure

Biosynthesis of catecholamines adrenaline (epinephrine) and noradrenaline (norepinephrine), intermediates DOPA and dopamine. Contribtued by NEUROtiker, CC-BY-SA 2.5 ( https://creativecommons.org/licenses/by-sa/2.5/ )

References

1.: Bhatt-Mehta V, Nahata MC. Dopamine and dobutamine in pediatric therapy. Pharmacotherapy. 1989;9(5):303-14. [PubMed: 2682552]
2.: De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, Brasseur A, Defrance P, Gottignies P, Vincent JL., SOAP II Investigators. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010 Mar 04;362(9):779-89. [PubMed: 20200382]
3.: Hornykiewicz O. A brief history of levodopa. J Neurol. 2010 Nov;257(Suppl 2):S249-52. [PubMed: 21080185]
4.: Ghadery C, Valli M, Mihaescu A, Strafella R, Navalpotro I, Kim J, Strafella AP. Molecular Imaging of Addictive Behavior in Idiopathic Parkinson’s Disease. Int Rev Neurobiol. 2018;141:365-404. [PubMed: 30314604]
5.: Blaschko H. The activity of l(-)-dopa decarboxylase. J Physiol. 1942 Nov 30;101(3):337-49. [PMC free article: PMC1393346] [PubMed: 16991567]
6.: Snyder SH. What dopamine does in the brain. Proc Natl Acad Sci U S A. 2011 Nov 22;108(47):18869-71. [PMC free article: PMC3223473] [PubMed: 22106252]
7.: CARLSSON A, LINDQVIST M, MAGNUSSON T. 3,4-Dihydroxyphenylalanine and 5-hydroxytryptophan as reserpine antagonists. Nature. 1957 Nov 30;180(4596):1200. [PubMed: 13483658]
8.: Abbott A. Neuroscience: the molecular wake-up call. Nature. 2007 May 24;447(7143):368-70. [PubMed: 17522649]
9.: MONTAGU KA. Catechol compounds in rat tissues and in brains of different animals. Nature. 1957 Aug 03;180(4579):244-5. [PubMed: 13451690]
10.: SANO I, GAMO T, KAKIMOTO Y, TANIGUCHI K, TAKESADA M, NISHINUMA K. Distribution of catechol compounds in human brain. Biochim Biophys Acta. 1959 Apr;32:586-7. [PubMed: 14441532]
11.: Carlsson A, Kehr W, Lindqvist M, Magnusson T, Atack CV. Regulation of monoamine metabolism in the central nervous system. Pharmacol Rev. 1972 Jun;24(2):371-84. [PubMed: 4564607]
12.: Haavik J, Toska K. Tyrosine hydroxylase and Parkinson’s disease. Mol Neurobiol. 1998 Jun;16(3):285-309. [PubMed: 9626667]
13.: Hardebo JE, Edvinsson L, Owman C, Rosengren E. Quantitative evaluation of the blood-brain barrier capacity to form dopamine from circulating L-DOPA. Acta Physiol Scand. 1977 Mar;99(3):377-84. [PubMed: 848309]
14.: Sibley DR, Monsma FJ, Shen Y. Molecular neurobiology of dopaminergic receptors. Int Rev Neurobiol. 1993;35:391-415. [PubMed: 8463063]
15.: David C, Fishburn CS, Monsma FJ, Sibley DR, Fuchs S. Synthesis and processing of D2 dopamine receptors. Biochemistry. 1993 Aug 17;32(32):8179-83. [PubMed: 8347618]
16.: Tank AW, Weiner H, Thurman JA. Enzymology and subcellular localization of aldehyde oxidation in rat liver. Oxidation of 3,4-dihydroxyphenylacetaldehyde derived from dopamine to 3,4-dihydroxyphenylacetic acid. Biochem Pharmacol. 1981 Dec 15;30(24):3265-75. [PubMed: 7034733]
17.: Kopin IJ. Catecholamine metabolism: basic aspects and clinical significance. Pharmacol Rev. 1985 Dec;37(4):333-64. [PubMed: 3915090]
18.: Meiser J, Weindl D, Hiller K. Complexity of dopamine metabolism. Cell Commun Signal. 2013 May 17;11(1):34. [PMC free article: PMC3693914] [PubMed: 23683503]
19.: Seamans JK, Yang CR. The principal features and mechanisms of dopamine modulation in the prefrontal cortex. Prog Neurobiol. 2004 Sep;74(1):1-58. [PubMed: 15381316]
20.: Meder D, Herz DM, Rowe JB, Lehéricy S, Siebner HR. The role of dopamine in the brain – lessons learned from Parkinson’s disease. Neuroimage. 2019 Apr 15;190:79-93. [PubMed: 30465864]
21.: Mills A. Dopamine: from Cinderella to Holy Grail. Trends Pharmacol Sci. 1992 Nov;13(11):399-400. [PubMed: 1440875]
22.: Beaulieu JM, Gainetdinov RR. The physiology, signaling, and pharmacology of dopamine receptors. Pharmacol Rev. 2011 Mar;63(1):182-217. [PubMed: 21303898]
23.: Andersen PH, Gingrich JA, Bates MD, Dearry A, Falardeau P, Senogles SE, Caron MG. Dopamine receptor subtypes: beyond the D1/D2 classification. Trends Pharmacol Sci. 1990 Jun;11(6):231-6. [PubMed: 2200181]
24.: Goldberg LI. Dopamine receptors and hypertension. Physiologic and pharmacologic implications. Am J Med. 1984 Oct 05;77(4A):37-44. [PubMed: 6148892]
25.: Velasco M, Luchsinger A. Dopamine: pharmacologic and therapeutic aspects. Am J Ther. 1998 Jan;5(1):37-43. [PubMed: 10099036]
26.: Montastruc JL, Chamontin B, Rostin M, Rascol O, Valet P, Gaillard G, Tran MA, Van TT, Ader JL, Montastruc P. Experimental and clinical approaches to treatment of hypertension by dopamine receptor agonists. Clin Exp Hypertens A. 1987;9(5-6):1069-84. [PubMed: 3304729]
27.: Feng J, Nestler EJ. Epigenetic mechanisms of drug addiction. Curr Opin Neurobiol. 2013 Aug;23(4):521-8. [PMC free article: PMC3644540] [PubMed: 23374537]
28.: Howes OD, McCutcheon R, Owen MJ, Murray RM. The Role of Genes, Stress, and Dopamine in the Development of Schizophrenia. Biol Psychiatry. 2017 Jan 01;81(1):9-20. [PMC free article: PMC5675052] [PubMed: 27720198]
29.: Wise RA. Addictive drugs and brain stimulation reward. Annu Rev Neurosci. 1996;19:319-40. [PubMed: 8833446]
30.: Wise RA. Drug-activation of brain reward pathways. Drug Alcohol Depend. 1998 Jun-Jul;51(1-2):13-22. [PubMed: 9716927]
31.: Jellinger KA. Post mortem studies in Parkinson’s disease–is it possible to detect brain areas for specific symptoms? J Neural Transm Suppl. 1999;56:1-29. [PubMed: 10370901]
32.: Root DH, Fabbricatore AT, Ma S, Barker DJ, West MO. Rapid phasic activity of ventral pallidal neurons during cocaine self-administration. Synapse. 2010 Sep;64(9):704-13. [PMC free article: PMC2904430] [PubMed: 20340176]
33.: Grattan DR. 60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-prolactin axis. J Endocrinol. 2015 Aug;226(2):T101-22. [PMC free article: PMC4515538] [PubMed: 26101377]
34.: Dobolyi A, Grattan DR, Stolzenberg DS. Preoptic inputs and mechanisms that regulate maternal responsiveness. J Neuroendocrinol. 2014 Oct;26(10):627-40. [PubMed: 25059569]
35.: Christine CW, Aminoff MJ. Clinical differentiation of parkinsonian syndromes: prognostic and therapeutic relevance. Am J Med. 2004 Sep 15;117(6):412-9. [PubMed: 15380498]
36.: Mink JW. Basal ganglia mechanisms in action selection, plasticity, and dystonia. Eur J Paediatr Neurol. 2018 Mar;22(2):225-229. [PMC free article: PMC5815934] [PubMed: 29396175]
37.: Perrin G, Papazian L, Martin C. [Dopexamine: a new dopaminergic agonist]. Ann Fr Anesth Reanim. 1993;12(3):308-20. [PubMed: 7902685]
38.: Gilbert JA, Frederick LM, Ames MM. The aromatic-L-amino acid decarboxylase inhibitor carbidopa is selectively cytotoxic to human pulmonary carcinoid and small cell lung carcinoma cells. Clin Cancer Res. 2000 Nov;6(11):4365-72. [PubMed: 11106255]
39.: Stoker TB, Torsney KM, Barker RA. Emerging Treatment Approaches for Parkinson’s Disease. Front Neurosci. 2018;12:693. [PMC free article: PMC6186796] [PubMed: 30349448]
40.: De Vecchis R, Ciccarelli A, Pucciarelli A. Unloading therapy by intravenous diuretic in chronic heart failure: a double-edged weapon? J Cardiovasc Med (Hagerstown). 2010 Aug;11(8):571-4. [PubMed: 20588135]
41.: Cho JR, Treweek JB, Robinson JE, Xiao C, Bremner LR, Greenbaum A, Gradinaru V. Dorsal Raphe Dopamine Neurons Modulate Arousal and Promote Wakefulness by Salient Stimuli. Neuron. 2017 Jun 21;94(6):1205-1219.e8. [PubMed: 28602690]
42.: Kittner SJ, Stern BJ, Feeser BR, Hebel R, Nagey DA, Buchholz DW, Earley CJ, Johnson CJ, Macko RF, Sloan MA, Wityk RJ, Wozniak MA. Pregnancy and the risk of stroke. N Engl J Med. 1996 Sep 12;335(11):768-74. [PMC free article: PMC1479545] [PubMed: 8703181]
43.: Yu XX, Fernandez HH. Dopamine agonist withdrawal syndrome: A comprehensive review. J Neurol Sci. 2017 Mar 15;374:53-55. [PubMed: 28104232]
44.: Colak T, Erdogan O, Yerebakan O, Arici C, Gurkan A. Symmetrical peripheral gangrene and dopamine. Ulus Travma Acil Cerrahi Derg. 2003 Jul;9(3):222-4. [PubMed: 12923702]
45.: Gelfman DM, Ornato JP, Gonzalez ER. Dopamine-induced increase in atrioventricular conduction in atrial fibrillation-flutter. Clin Cardiol. 1987 Nov;10(11):671-3. [PubMed: 3677500]

: Disclosure: James Sonne declares no relevant financial relationships with ineligible companies.
: Disclosure: Amandeep Goyal declares no relevant financial relationships with ineligible companies.
: Disclosure: Wilfredo Lopez-Ojeda declares no relevant financial relationships with ineligible companies.

Dopamine – StatPearls – NCBI Bookshelf

Continuing Education Activity

Objectives:

Identify the mechanism of action at various doses of dopamine.
Review the indications for therapy with dopamine.
Outline the potential adverse effects of dopamine therapy.
Summarize the importance of interprofessional communication and improving care coordination among the interprofessional team when initiating dopamine therapy.

Access free multiple choice questions on this topic.

Indications

Mechanism of Action

If an individual regularly consumes L-tyrosine in abundance, it readily crosses the blood-brain barrier, as does L-DOPA.[13]. But its utility is spatially restricted because DA cannot cross the blood-brain barrier. However, if L-tyrosine levels are low, L-phenylalanine may be converted into L-tyrosine by phenylalanine hydroxylase.

Once in the synaptic cleft, DA is transported back into the pre-synaptic neuron via DA transporters (DAT) for repackaging or can remain in the extracellular space to be taken up by glial cells or metabolized by the cellular membrane. DA may be metabolized extraneuronally by catechol-o-methyltransferase (COMT) to 3-methoxytyramine (3-MT), while monoamine oxidase-B (MAO-B) will rapidly metabolize 3-MT to homovanillic acid (HVA). [16][17] Alternatively, it may undergo metabolism inside the cytoplasm, where the dual action of MAO-A and aldehyde dehydrogenase (ALDH) will convert DA to the phenolic acid 3, 4-dihydroxyphenylacetic acid (DOPAC).[18]

As indicated earlier, the systemic action of DA is subject to mediation by various receptors (D1, D2, D3, D4, and D5) and the alpha- and beta-adrenergic receptors. These G-coupled receptors generally group as either D1 or D2, primarily based on their traditional biochemical functions showing that dopamine can modulate adenylyl cyclase activity. [6][20] However, based on their molecular structure, biochemical properties, and pharmacological functions, DA receptors are further classified either as D1-class (D1 and D5) or D2-class (D2, D3, D4).[21][22][23][15]

Administration

Adverse Effects

Contraindications

Monitoring

Toxicity

Enhancing Healthcare Team Outcomes

Review Questions

Access free multiple choice questions on this topic.
Comment on this article.

Figure

References

1.: Bhatt-Mehta V, Nahata MC. Dopamine and dobutamine in pediatric therapy. Pharmacotherapy. 1989;9(5):303-14. [PubMed: 2682552]
2.: De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, Brasseur A, Defrance P, Gottignies P, Vincent JL., SOAP II Investigators. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010 Mar 04;362(9):779-89. [PubMed: 20200382]
3.: Hornykiewicz O. A brief history of levodopa. J Neurol. 2010 Nov;257(Suppl 2):S249-52. [PubMed: 21080185]
4.: Ghadery C, Valli M, Mihaescu A, Strafella R, Navalpotro I, Kim J, Strafella AP. Molecular Imaging of Addictive Behavior in Idiopathic Parkinson’s Disease. Int Rev Neurobiol. 2018;141:365-404. [PubMed: 30314604]
5.: Blaschko H. The activity of l(-)-dopa decarboxylase. J Physiol. 1942 Nov 30;101(3):337-49. [PMC free article: PMC1393346] [PubMed: 16991567]
6.: Snyder SH. What dopamine does in the brain. Proc Natl Acad Sci U S A. 2011 Nov 22;108(47):18869-71. [PMC free article: PMC3223473] [PubMed: 22106252]
7.: CARLSSON A, LINDQVIST M, MAGNUSSON T. 3,4-Dihydroxyphenylalanine and 5-hydroxytryptophan as reserpine antagonists. Nature. 1957 Nov 30;180(4596):1200. [PubMed: 13483658]
8.: Abbott A. Neuroscience: the molecular wake-up call. Nature. 2007 May 24;447(7143):368-70. [PubMed: 17522649]
9.: MONTAGU KA. Catechol compounds in rat tissues and in brains of different animals. Nature. 1957 Aug 03;180(4579):244-5. [PubMed: 13451690]
10.: SANO I, GAMO T, KAKIMOTO Y, TANIGUCHI K, TAKESADA M, NISHINUMA K. Distribution of catechol compounds in human brain. Biochim Biophys Acta. 1959 Apr;32:586-7. [PubMed: 14441532]
11.: Carlsson A, Kehr W, Lindqvist M, Magnusson T, Atack CV. Regulation of monoamine metabolism in the central nervous system. Pharmacol Rev. 1972 Jun;24(2):371-84. [PubMed: 4564607]
12.: Haavik J, Toska K. Tyrosine hydroxylase and Parkinson’s disease. Mol Neurobiol. 1998 Jun;16(3):285-309. [PubMed: 9626667]
13.: Hardebo JE, Edvinsson L, Owman C, Rosengren E. Quantitative evaluation of the blood-brain barrier capacity to form dopamine from circulating L-DOPA. Acta Physiol Scand. 1977 Mar;99(3):377-84. [PubMed: 848309]
14.: Sibley DR, Monsma FJ, Shen Y. Molecular neurobiology of dopaminergic receptors. Int Rev Neurobiol. 1993;35:391-415. [PubMed: 8463063]
15.: David C, Fishburn CS, Monsma FJ, Sibley DR, Fuchs S. Synthesis and processing of D2 dopamine receptors. Biochemistry. 1993 Aug 17;32(32):8179-83. [PubMed: 8347618]
16.: Tank AW, Weiner H, Thurman JA. Enzymology and subcellular localization of aldehyde oxidation in rat liver. Oxidation of 3,4-dihydroxyphenylacetaldehyde derived from dopamine to 3,4-dihydroxyphenylacetic acid. Biochem Pharmacol. 1981 Dec 15;30(24):3265-75. [PubMed: 7034733]
17.: Kopin IJ. Catecholamine metabolism: basic aspects and clinical significance. Pharmacol Rev. 1985 Dec;37(4):333-64. [PubMed: 3915090]
18.: Meiser J, Weindl D, Hiller K. Complexity of dopamine metabolism. Cell Commun Signal. 2013 May 17;11(1):34. [PMC free article: PMC3693914] [PubMed: 23683503]
19.: Seamans JK, Yang CR. The principal features and mechanisms of dopamine modulation in the prefrontal cortex. Prog Neurobiol. 2004 Sep;74(1):1-58. [PubMed: 15381316]
20.: Meder D, Herz DM, Rowe JB, Lehéricy S, Siebner HR. The role of dopamine in the brain – lessons learned from Parkinson’s disease. Neuroimage. 2019 Apr 15;190:79-93. [PubMed: 30465864]
21.: Mills A. Dopamine: from Cinderella to Holy Grail. Trends Pharmacol Sci. 1992 Nov;13(11):399-400. [PubMed: 1440875]
22.: Beaulieu JM, Gainetdinov RR. The physiology, signaling, and pharmacology of dopamine receptors. Pharmacol Rev. 2011 Mar;63(1):182-217. [PubMed: 21303898]
23.: Andersen PH, Gingrich JA, Bates MD, Dearry A, Falardeau P, Senogles SE, Caron MG. Dopamine receptor subtypes: beyond the D1/D2 classification. Trends Pharmacol Sci. 1990 Jun;11(6):231-6. [PubMed: 2200181]
24.: Goldberg LI. Dopamine receptors and hypertension. Physiologic and pharmacologic implications. Am J Med. 1984 Oct 05;77(4A):37-44. [PubMed: 6148892]
25.: Velasco M, Luchsinger A. Dopamine: pharmacologic and therapeutic aspects. Am J Ther. 1998 Jan;5(1):37-43. [PubMed: 10099036]
26.: Montastruc JL, Chamontin B, Rostin M, Rascol O, Valet P, Gaillard G, Tran MA, Van TT, Ader JL, Montastruc P. Experimental and clinical approaches to treatment of hypertension by dopamine receptor agonists. Clin Exp Hypertens A. 1987;9(5-6):1069-84. [PubMed: 3304729]
27.: Feng J, Nestler EJ. Epigenetic mechanisms of drug addiction. Curr Opin Neurobiol. 2013 Aug;23(4):521-8. [PMC free article: PMC3644540] [PubMed: 23374537]
28.: Howes OD, McCutcheon R, Owen MJ, Murray RM. The Role of Genes, Stress, and Dopamine in the Development of Schizophrenia. Biol Psychiatry. 2017 Jan 01;81(1):9-20. [PMC free article: PMC5675052] [PubMed: 27720198]
29.: Wise RA. Addictive drugs and brain stimulation reward. Annu Rev Neurosci. 1996;19:319-40. [PubMed: 8833446]
30.: Wise RA. Drug-activation of brain reward pathways. Drug Alcohol Depend. 1998 Jun-Jul;51(1-2):13-22. [PubMed: 9716927]
31.: Jellinger KA. Post mortem studies in Parkinson’s disease–is it possible to detect brain areas for specific symptoms? J Neural Transm Suppl. 1999;56:1-29. [PubMed: 10370901]
32.: Root DH, Fabbricatore AT, Ma S, Barker DJ, West MO. Rapid phasic activity of ventral pallidal neurons during cocaine self-administration. Synapse. 2010 Sep;64(9):704-13. [PMC free article: PMC2904430] [PubMed: 20340176]
33.: Grattan DR. 60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-prolactin axis. J Endocrinol. 2015 Aug;226(2):T101-22. [PMC free article: PMC4515538] [PubMed: 26101377]
34.: Dobolyi A, Grattan DR, Stolzenberg DS. Preoptic inputs and mechanisms that regulate maternal responsiveness. J Neuroendocrinol. 2014 Oct;26(10):627-40. [PubMed: 25059569]
35.: Christine CW, Aminoff MJ. Clinical differentiation of parkinsonian syndromes: prognostic and therapeutic relevance. Am J Med. 2004 Sep 15;117(6):412-9. [PubMed: 15380498]
36.: Mink JW. Basal ganglia mechanisms in action selection, plasticity, and dystonia. Eur J Paediatr Neurol. 2018 Mar;22(2):225-229. [PMC free article: PMC5815934] [PubMed: 29396175]
37.: Perrin G, Papazian L, Martin C. [Dopexamine: a new dopaminergic agonist]. Ann Fr Anesth Reanim. 1993;12(3):308-20. [PubMed: 7902685]
38.: Gilbert JA, Frederick LM, Ames MM. The aromatic-L-amino acid decarboxylase inhibitor carbidopa is selectively cytotoxic to human pulmonary carcinoid and small cell lung carcinoma cells. Clin Cancer Res. 2000 Nov;6(11):4365-72. [PubMed: 11106255]
39.: Stoker TB, Torsney KM, Barker RA. Emerging Treatment Approaches for Parkinson’s Disease. Front Neurosci. 2018;12:693. [PMC free article: PMC6186796] [PubMed: 30349448]
40.: De Vecchis R, Ciccarelli A, Pucciarelli A. Unloading therapy by intravenous diuretic in chronic heart failure: a double-edged weapon? J Cardiovasc Med (Hagerstown). 2010 Aug;11(8):571-4. [PubMed: 20588135]
41.: Cho JR, Treweek JB, Robinson JE, Xiao C, Bremner LR, Greenbaum A, Gradinaru V. Dorsal Raphe Dopamine Neurons Modulate Arousal and Promote Wakefulness by Salient Stimuli. Neuron. 2017 Jun 21;94(6):1205-1219.e8. [PubMed: 28602690]
42.: Kittner SJ, Stern BJ, Feeser BR, Hebel R, Nagey DA, Buchholz DW, Earley CJ, Johnson CJ, Macko RF, Sloan MA, Wityk RJ, Wozniak MA. Pregnancy and the risk of stroke. N Engl J Med. 1996 Sep 12;335(11):768-74. [PMC free article: PMC1479545] [PubMed: 8703181]
43.: Yu XX, Fernandez HH. Dopamine agonist withdrawal syndrome: A comprehensive review. J Neurol Sci. 2017 Mar 15;374:53-55. [PubMed: 28104232]
44.: Colak T, Erdogan O, Yerebakan O, Arici C, Gurkan A. Symmetrical peripheral gangrene and dopamine. Ulus Travma Acil Cerrahi Derg. 2003 Jul;9(3):222-4. [PubMed: 12923702]
45.: Gelfman DM, Ornato JP, Gonzalez ER. Dopamine-induced increase in atrioventricular conduction in atrial fibrillation-flutter. Clin Cardiol. 1987 Nov;10(11):671-3. [PubMed: 3677500]

: Disclosure: James Sonne declares no relevant financial relationships with ineligible companies.
: Disclosure: Amandeep Goyal declares no relevant financial relationships with ineligible companies.
: Disclosure: Wilfredo Lopez-Ojeda declares no relevant financial relationships with ineligible companies.

How the hormone dopamine affects the body and human behavior

About how a change in the concentration of the hormone dopamine in the human body helps to quit smoking, provokes the emergence of gambling addiction and shopaholism, causes myopia, and also contributes to the fight against cancerous tumors, says the science department of Gazeta. Ru.

Dopamine is an active chemical produced by the human brain and a hormone produced by the adrenal glands. Dopamine is naturally produced during processes that a person enjoys, which is why this substance is used by the brain to evaluate and reinforce actions that are important for later life.

Dopamine agonists, substances that stimulate dopamine receptors and increase the production of the hormone, are used to improve certain conditions, such as Parkinson’s disease. Scientists are conducting numerous studies aimed at clarifying the role of dopamine in other processes – the formation of various addictions, cancer treatment, and even smoking cessation.

Smoking without a cigarette is dangerous to health

Since it is not nicotine that causes cancer, but chemicals – carcinogens – released by a cigarette …

Nov 03 18:50

Gene helps quit smoking

The presence in human DNA of a specific variant of the Taq1A gene called Taq1A A2/A2 can have a direct impact on a person’s ability to stop smoking. The study by an international team of scientists led by Ma Yunlong of Zhejiang University School of Medicine was published Tuesday night in Translational Psychiatry and in Nature .

The Taq1A A2/A2 gene encodes the work of dopamine receptors, thereby changing the degree of their activity. An excess amount of dopamine in the human brain, in turn, contributes to the formation of nicotine addiction – the brain begins to “realize” that smoking brings pleasure, which means that it is an action that needs to be repeated.

Scientists analyzed the results of 22 studies containing data on 11,075 people, 9487 of whom were Caucasians. The authors of the work claim that they were able to detect a pattern:

Caucasians whose DNA carried a specific variant of the Taq1A gene (Taq1A A2/A2) were much more likely to successfully cope with nicotine addiction and stop smoking than those who possessed the Taq1A A1/A1 or Taq1A A1/A2 genes.

The authors of the study emphasize that their work needs further verification, and it is too early to apply the findings in practical medicine.

Parkinson’s handwriting is recognized

Israeli scientists used an automatic handwriting analysis system to diagnose…

February 25 17:30

Gambling is a side effect of treatment

Another group of researchers found that physicians had long overestimated the effectiveness of dopamine agonists when using them to combat Parkinson’s disease and psychiatric disorders.

Agonist drugs act on dopamine receptors, causing them to work more actively. An excess amount of the hormone provoked the formation of various mental disorders and addictions.

Thus, over the course of ten years in 21 countries of the world, 1580 cases of addictions as a result of side effects of drugs were recorded. These cases included

628 episodes of gambling addiction, 465 cases of hypersexuality and 202 cases of shopaholism. Of the 1,580 diagnoses made, 710 owed their occurrence to dopamine receptor agonists, 90,003 to 90,004, and the remaining 870 to all other types of drugs that affect the hormonal background. More details about the study can be found in JAMA Internal Medicine .

Our whole life is the fight against cancer

Aging and bad habits weaken the body and allow cancer to triumph over healthy tissues …

July 26 11:55

Dopamine against cancer

But researchers from Ohio State University, led by Sujita Basu, still advise using dopamine as a cure – albeit for cancer. The corresponding article was published in the International Journal of Cancer .

Scientists have stated that

the use of dopamine significantly slows down the growth of blood vessels in a malignant tumor, and this is one of the most important factors in its growth, since blood vessels provide nutrition to the cancer.

In addition, the researchers claim that the use of dopamine reduces the negative effect of the drug 5-fluorouracil (an anticancer drug used in chemotherapy) on the patient’s blood composition.

“Lenses in which you can sleep are the biggest evil”

About what eye diseases lie in wait for us today, what is the danger of small screens and how . ..

July 17 15:56

No dopamine – there will be myopia

This summer, scientists announced that they were able to find out the real cause of myopia in modern teenagers. An article about the work of researchers was published in the journal Nature.

In recent decades, myopia has taken on the character of an epidemic: in Europe and the United States, the number of myopic people has more than doubled over the past century, and in Asian countries the situation is even worse. So, if 60 years ago 10–20% of Chinese suffered from myopia, now there are already 9 of them.0%. In Seoul, 95.6% of 19-year-olds are nearsighted.

Over the years, physicians have investigated the causes of myopia, which is caused by the elongation of the eyeball and focusing the image in front of the retina rather than on it. In the course of the work, it turned out that neither genetics nor the habit of modern people to spend a lot of time reading and in front of monitors of electronic devices are the decisive causes of the onset of the disease: the authors of the study stated that myopia is caused by a lack of daylight.

Modern people began to spend much less time on the street, and this is what provokes the occurrence of myopia, since under the influence of bright daylight the retina produces dopamine, and its lack causes the lengthening of the eyeball.

Doctors have calculated that in order to maintain good vision, a person needs to spend at least three hours a day in illumination of 10,000 lux (the brightness of sunlight), while the most powerful illumination achievable indoors usually does not exceed 5,000 lux.

Ways to boost dopamine levels and increase productivity – I Love Supersport Blog

How about a light dope to increase mood and productivity? No, no pills and banned substances! It’s all about dopamine – that very powerful neurotransmitter that is responsible for your performance and desire for life.

High dopamine = high performance

What is dopamine? Dopamine is a neurotransmitter that our brain produces to push us to do something. This is the main reason why we can focus and achieve great results, even if the benefits are not immediate or obvious.

Dopamine cannot be taken like magic pills – our brain produces it on its own. But there are simple ways to help him and increase the level of dopamine in the body to stay focused, productive and motivated.

In addition to the fact that a constant supply of dopamine in your body is the main motivator, it provides a few more additional bonuses:

📌 Helps to reduce weight
📌 Makes life more vivid
📌 Improves memory
📌 Stops self-destructive behavior, including some types of addiction
📌 Fights depression
📌 Helps counter impulsive behavior
📌 Helps prevent Parkinson’s disease

If you want to be productive and achieve your goals while staying positive, check out our ways to get your dopamine levels down ❤️

1. Sun

We often hear that fresh air improves mood, and this really makes sense. Exposure to sunlight increases the number of dopamine receptors and produces vitamin D , which in turn activates genes that help release dopamine. In fact, any light causes a release of dopamine in your eyes, which is probably why we like to “stick” in front of device screens.

2. Communication

Man is a social being, and this is inherent in us by nature. Contact with another person causes the production of dopamine not only in you, but also in this person. So get your dose of dopamine by talking to your loved ones, hugging your kids, or even shaking hands with co-workers. Even if you consider yourself an introvert, occasional contact with people, including physical ones, can be a good mood booster.

3. Massage

In fact, dopamine levels are also increased by other touch-heavy activities, including massage. We probably don’t need to convince you to get a massage, since you already know that it reduces stress and muscle tension. But if you haven’t done it for a long time, it’s time to visit a local salon.

4. Animals

The principle of increasing dopamine through touch extends to animals, so don’t forget to pet or hug your pets. They need it just as much as you do! But this applies more to mammals, so it works with dogs, cats and even rabbits.

5. Sleep

People become irritable from lack of sleep. One reason is that lack of sleep reduces the number of dopamine receptors. Less dopamine means worse mood.

Of course, the optimal amount of sleep is a matter of debate, but we recommend trying waking up without an alarm to find out how much sleep you personally need. And yes, invest in a good bed. You spend a third of your life on it!

6. Meditation

Sometimes the best way to do something is to do nothing. Namely, do nothing physically, while trying to balance your thoughts. Meditation or just self-reflection is also associated with an increase in dopamine levels.

7. Something new

Dopamine production is triggered when we see something new and exciting in front of us. Our ancestors experienced this feeling when they discovered new herds to hunt or new plants to harvest. Under the current conditions, it will probably be difficult for us to do this. But we have internet!

The Internet is a godsend for finding new music for new videos. A simple dopamine booster is looking for inspiration on Pinterest or even online stores. But don’t go overboard with it!

It’s better to try something new every day—read a random wiki article or even take a different route to work. Turning a block earlier will take you down an unfamiliar path, and this will help your brain wake up.

8. Music

Studies have shown that when we listen to music we really like, the brain releases dopamine. Good music activates pleasure centers in the same way that good food does. That’s another reason to put together a playlist of your favorite tracks so you can quickly cheer yourself up just by putting on your headphones.

But even if you don’t have music on hand, the “anticipation” of melodies and lyrics actually has the same effect. If you get excited when your favorite song’s intro plays, it’s because you’re anticipating the chorus. All the same parts of the brain work. This is also the reason why we love to hum to ourselves and play the song we hear in our head, whether we like it or not.

If we talk about singing, then creating and performing music also has its payoff. In particular, it is also a way to get a dose of dopamine. So brush up on your piano lessons and bring your guitar up from the attic.

9. Creativity

When diving deep into creative work, have you ever noticed going into a state of hyperfocus, where you feel like you can do anything? This state is called flow, and dopamine helps achieve it.

You can increase dopamine levels by simply engaging in creative hobbies such as photography, writing stories, or drawing.

10. A hobby that requires attention to detail

Another way to increase dopamine levels is to take up a hobby. But not just a hobby, it should be something that requires focus. It can be anything from assembling LEGO sets to repairing a car.

11. Task management

Dopamine is released after you complete something, be it a large amount of work or a small task. It follows that if you want more dopamine “bursts”, break big jobs into smaller tasks.

The secret is that you need to write down these tasks. Not to forget them – just from the point of view of dopamine production, it is much more pleasant to physically cross something off the list. There is nothing more satisfying than marking a task as completed. The brain rejoices in these moments.

12. Strike

A strike is a visual reminder of how many times you have achieved something in a row. In games, the strike is often used to track wins, and in everyday affairs, it can become an additional stimulus for you to produce dopamine.

The easiest way is to take a calendar and put a cross on it every day when you do something (like clean your desk or eat a healthy lunch). Soon you will have a neat row of crosses that will fold into a line. It is called a strike.

This method increases the production of dopamine in the same way as completing a task. Until you have reached your final goal, just knowing the right path you have chosen causes your brain to produce enough dopamine to keep going.

13. Victory Celebration

We all love to win in part because victory celebration stimulates the release of dopamine in our bodies. Even if you’re not the type to do a victory dance in the office after a successful email, you can still celebrate success in other ways.

Share achievements with friends in the chat. Write on the sticker “I did it!” and stick to your monitor. Show a victory gesture with your fist. All of these activities will help cement your sense of satisfaction, so you’re sure to get a dopamine rush the next time you achieve something.

14. Cold shower

If you live in a cold area, taking an ice cold shower is not at all pleasant. However, it can increase dopamine levels by as much as 250%. A cold shower gives an invigorating impulse. First you need to overcome the feeling of cold, and soon you will prefer it to your usual temperature.

15. Weight loss

Dopamine itself helps to lose weight. But the opposite is also true: when you lose weight, dopamine levels increase. This is because being overweight reduces the number of dopamine receptors.

The good news is that if you start to lose weight, these receptors will return and, as a result, will help you increase your dopamine levels. This efficient cycle will help you reach your ideal weight!

16. Workouts

We can’t help but say that. I Love Supersport often writes about how exercise helps relieve stress and increase productivity. This is because your body craves physical activity (even if your brain sometimes hates it). And to make it more fun, the brain releases fun chemicals like serotonin, endorphins, and, yes, dopamine.

There are also light exercises that can help increase dopamine levels. Try taking your dog out for a run, climbing the stairs, or playing video sports equipment. But it is better to make training regular by choosing a sport to your liking.

17. Walks

If you still don’t have the opportunity to include any intense exercise in your day, you can simply walk around the area. Walking makes blood flow through the vessels and muscles move, which is why it is considered exercise, which means it also causes the production of dopamine.

Even if you hate walking, try incorporating it into your daily routine and pretty soon you’ll be prioritizing parking spaces away from your office for the chance to walk.

Next, food-related ways to increase dopamine. This is a big and important block, because the trace elements that we get from food are directly related to dopamine.

18. Tyrosine

Tyrosine is the building block of dopamine, so make sure you get enough of this protein. Luckily, it’s easy enough to find. Common foods high in tyrosine include:

– Almonds
– Avocados
– Bananas
– Beef
– Chicken
– Chocolate
– Coffee
– Eggs
– Green Tea
– Milk 9010 7 – Watermelon
– Yogurt

19. Phenylalanine

Phenylalanine is an amino acid, “building block” of protein. It is used for chronic pain, depression, attention deficit hyperactivity disorder (ADHD), Parkinson’s disease, rheumatoid arthritis, osteoarthritis, and a skin condition called vitiligo. The body uses phenylalanine to create chemical messengers such as dopamine. Phenylalanine can be found in most protein-containing foods such as:

– Dairy
– Eggs
– Fish
– Meat
– Nuts
– Seeds
– Soy products

20. Caffeine

Most of us have experienced powerful effect of caffeine on productivity. It not only copes with lethargy, but also increases the release of dopamine, especially in the area of our brain that is associated with attention and concentration. You can get your dose of caffeine from:

– Coffee
– Tea
– Chocolate, preferably dark

21. Pregnenolone

This happiness chemical not only boosts dopamine levels, but is also a building block for our body’s hormones. Another great thing about pregnenolone is that, like dopamine, it helps lift your mood.

The good news is that finding pregnenolone-boosting foods is easy because pregnenolone is made up of cholesterol. It can be obtained from:

– Oils
– Dairy products
– Eggs
– Meats

In addition, the liver itself produces cholesterol, which, in turn, supplies you with pregnenolone.

22. Resveratrol

Resveratrol is an antioxidant that helps increase dopamine levels in the brain. As an antioxidant, it also helps fight cancer, heart disease, and diabetes. You can get it from:

– Blueberries
– Cranberries
– Cocoa
– Dark Chocolate
– Grapes
– Peanuts
– Pistachios
– Wine – in moderation, of course.

23. DHA

DHA (docosahexaenoic acid) is used to treat dementia, type 2 diabetes, coronary heart disease, and ADHD. It is also used to prevent and treat depression. DHA increases dopamine levels by supporting the brain’s electrical signals and decreasing the production of an enzyme that breaks down dopamine. DHA can be found in:

– Herring
– Lake Trout
– Mackerel
– Salmon
– Sardine
– Seaweed

24. Carvacrol

Carvacrol is another chemical that stimulates dopamine synthesis when taken in low doses. It also protects your liver, fights bacteria, and acts as an antidepressant. Carvacrol is found in:

– Oregano
– Marsilia
– Thyme Oil
– Wild Bergamot

25. Folic Acid

Folic acid helps the body build cells and fight heart disease. In addition, it releases serotonin, which is involved in the regulation of brain processes such as memory, anxiety, depression, aggression, mood, appetite, sleep, emotions, and perception. You can get it from:

– Dark green leafy vegetables such as cabbage and spinach
– Fruit
– Fruit juice
– Meat
– Nuts
– Poultry

26. Monounsaturated fats 9001 5

Monounsaturated fats are fatty acids that are considered beneficial for heart, as they reduce the risk of cardiovascular disease. One study found that more monounsaturated fats helped improve mood and reduce anger and irritability. Monounsaturated fats are commonly found in:

– Avocado
– Rapeseed oil
– Walnuts
– Olive oil
– Peanut oil

27. Butyrates

Butyrates what you think!) are extremely important for intestinal health. An unhealthy gut can affect mental health, weight, mood, and a range of other digestive disorders. Butyrates are beneficial for the brain and nerve cells as they prevent the death of the latter responsible for activating movement. They are also used to treat anxiety and depression, as they affect processes in the hippocampus, the part of the brain responsible for emotions and emotional memory. Butyrates can be found in:

– Butter
– Milk
– Vegetable oils

28. Uridine

Uridine helps restore dopamine balance by promoting the creation of new dopamine receptors in the brain. It can be used to treat nervous disorders, as well as to improve memory. Dietary sources of uridine are:

Beer
Broccoli
Chinese cabbage
Fish
Mushrooms
Oats
Parsley

29. Avoid sweeteners

While sugar does give you a dopamine spike, it is considered unhealthy and addictive. Also avoid aspartame. It has been found to lower dopamine levels in your brain and also blunts serotonin, another chemical we need to feel good.

30. Less lipopolysaccharides

This word is hard to pronounce, but it’s good because you should avoid it. Lipopolysaccharides are also called endotoxins, and yes, they are indeed toxins. In fact, their excess disables the immune system. More importantly, they suppress dopamine production.

The best way to deal with this is to maintain a balance of “good” and “bad” bacteria in your gut. How to do it?

– Eat plenty of probiotic foods, mostly fermented, such as yogurt, kefir, and kimchi.
– Sleep enough hours to live in the same biorhythm with your intestines.
– Do not abuse fatty and sweet foods. It consists of lipids and polysaccharides, the less of them, the less endotoxins.

31. Supplements

Although you can’t pump dopamine into your brain, at least until homemade brain injection kits are invented, you can take supplements to stimulate more dopamine production. These include:

– Curcumin, the active ingredient in our favorite curry seasoning, turmeric, helps boost dopamine levels.
– Ginkgo biloba is a popular miracle pill that can increase dopamine levels by keeping it in your brain longer, although this has not yet been scientifically proven.
– L-theanine increases the production of neurotransmitters in the brain, one of which is dopamine.