Dopamine
Episodes
In this clip, Dr. Andrew Huberman discusses the power of effort, dopamine in motivation, and the mindset needed for effective learning and growth.
In this clip, Dr. Andrew Huberman discusses dopamine's role in motivation and strategies for maintaining stable levels.
In this clip, Dr. Andrew Huberman discusses using negative visualization, discomfort, and cold exposure to overcome procrastination and boost motivation.
-
In this clip, Dr. Andrew Huberman discusses the power of effort, dopamine in motivation, and the mindset needed for effective learning and growth.
-
In this clip, Dr. Andrew Huberman discusses dopamine's role in motivation and strategies for maintaining stable levels.
-
In this clip, Dr. Andrew Huberman discusses using negative visualization, discomfort, and cold exposure to overcome procrastination and boost motivation.
-
In this clip, Dr. Andrew Huberman discusses social media's dopamine effects, usage limits, and its impact on relationships and ADHD.
-
In this clip, Dr. Andrew Huberman discusses how caffeine and other stimulants impact the release of dopamine in the brain.
-
Dr. Andrew Huberman discusses the role of dopamine in driving motivation and offers practical tools for enhancing mood and focus.
-
In this clip, Dr. Giselle Petzinger discusses how no evidence exists that lifestyle factors, such as diet and exercise, can cure Parkinson's disease or obviate the need for dopamine replacement.
-
In this clip, Dr. Giselle Petzinger discusses how intense exercise can impact motor scores in people with Parkinson's disease.
-
In this clip, Dr. Giselle Petzinger explains that strenuous exercise affects dopamine sensitivity in the brains of people with Parkinson's disease.
-
In this clip, Dr. Giselle Petzinger highlights some of the risk factors for Parkinson's disease, and discusses how this is likely a multifaceted problem.
-
How loss of dopamine-producing neurons affects brain circuitry and behavior | Giselle Petzinger ClipIn this clip, Dr. Giselle Petzinger explains how the loss of dopamine disrupts circuitry in the brains of people with Parkinson's disease.
-
Dr. Giselle Petzinger discusses new findings in Parkinson's disease research, emphasizing exercise's role in delaying disease progression.
Topic Pages
News & Publications
-
Vitamin D shapes neurodevelopment, influencing the development of dopamine-producing neurons and, ultimately, the risk of schizophrenia. onlinelibrary.wiley.com
Vitamin D plays a crucial role in the early development of dopamine-producing neurons, shedding light on the potential neurodevelopmental origins of schizophrenia. Abnormalities in dopamine signaling are at the heart of this complex mental health disorder, and a recent study suggests that vitamin D deficiency during pregnancy influences these pathways, increasing the risk of schizophrenia in offspring.
Researchers examined nerve growth, synapse formation, and dopamine release in various dopamine-producing cells exposed to vitamin D over time. They focused on SH-SY5Y cells—which can mature into dopaminergic (dopamine-releasing) neurons—and other brain cells.
They found that vitamin D increased neuron outgrowth and branching in dopaminergic cells, enhancing the production and release of dopamine. It also altered the expression and distribution of critical presynaptic proteins involved in dopamine release, further supporting its role in dopaminergic development.
These findings suggest vitamin D is crucial for developing and maturing dopamine-producing neurons. They provide new insights into how maternal vitamin D levels might influence the risk of schizophrenia in offspring by affecting early dopamine signaling pathways. Evidence suggests that vitamin D synergizes with omega-3 fatty acids to support neurodevelopment. Learn more about this relationship in this peer-reviewed article coauthored by Dr. Rhonda Patrick.
-
Maternal vitamin D deficiency linked to potential developmental disorders, emphasizing a role in dopamine signaling. neurosciencenews.com
Dopamine is a neurotransmitter best known for its role in motor, motivation, and pleasure control. A new study highlights vitamin D’s influence on dopamine signaling and emphasizes its essential role in the normal development of dopamine-producing cells.
Researchers developed three cell lines to mimic the natural process of embryonic development, during which cells differentiate (specialize) into dopamine-producing neurons. Then they cultured the cells in the presence or absence of vitamin D.
They found that vitamin D participated in neuronal growth and branching, the rearrangement of presynaptic proteins, and the production and release of dopamine. The researchers posited that glial-derived growth factor, a vitamin D-dependent factor that promotes dopamine neuron differentiation, was the mechanism driving these effects.
These findings suggest that vitamin D plays multiple roles in dopamine signaling, with potential implications for neurodevelopmental disorders like schizophrenia, ADHD, and autism. They also underscore the importance of adequate maternal vitamin D status during pregnancy.
Interestingly, vitamin D and omega-3 fatty acids may synergistically work to support neurodevelopment further. Read this open-access peer-reviewed article by Dr. Rhonda Patrick to learn more.
-
Gut microbes may drive the motivation to exercise. medicalxpress.com
Microbes in your gut may trigger your motivation to exercise, a new study in mice has found. Compounds produced by the microbes signal the release of dopamine – a neurotransmitter produced in the brain that promotes the “runner’s high” and the desire to exercise.
Researchers analyzed the gut microbial species and the byproducts of their metabolism from nearly 200 mice with diverse genetic backgrounds. They also tracked the animals' daily exercise activity and measured their endurance.
They found that mice that had certain species of gut microbes – Eubacterium rectale and Coprococcus eutactus – exercised more and had greater endurance than mice lacking these microbes. These two species produce compounds called fatty acid amides, which interact with gut neurons and ultimately activate dopamine-producing neurons in the brain, turning on the brain’s reward circuits and triggering the desire to exercise00394-0.pdf).
This study in mice reveals a novel way in which the gut microbiome influences human health and behavior. It may also provide evidence to support the use of therapeutic microbial transfer to promote exercise behavior and improve aspects of mood.
-
Gut microbes may play a role in controlling the motivation to exercise by modulating runner's high www.sciencedaily.com
Microbes in your gut may trigger your motivation to exercise, a new study in mice has found. Compounds produced by the microbes signal the release of dopamine – a neurotransmitter produced in the brain that promotes the “runner’s high” and the desire to exercise.
Researchers analyzed the gut microbial species and the byproducts of their metabolism from nearly 200 mice with diverse genetic backgrounds. They also tracked the animals' daily exercise activity and measured their endurance.
They found that mice that had certain species of gut microbes – Eubacterium rectale and Coprococcus eutactus – exercised more and had greater endurance than mice lacking these microbes. These two species produce compounds called fatty acid amides, which interact with gut neurons and ultimately activate dopamine-producing neurons in the brain, turning on the brain’s reward circuits and triggering the desire to exercise.
This study in mice reveals a novel way in which the gut microbiome influences human health and behavior. It may also provide evidence to support the use of therapeutic microbial transfer to promote exercise behavior and improve aspects of mood.
-
Insulin improves dopamine signaling in regions of the brain associated with eating behavior. www.sciencedaily.com
Insulin signaling in the brain influences behavior, weight regulation, motivation, and cognition. Previous research demonstrates that insulin resistance reduces brain volume and cognitive function in middle-aged adults. Results of a new study demonstrate that insulin interacts with dopamine to modulate reward-based behavior and whole-body metabolism.
Dopamine is a neurotransmitter that regulates activity of the mesocorticolimbic system, a region of the brain involved in reward-based learning. Mesocorticolimbic circuits transmit information from the midbrain to the ventral and dorsal striatum, prefrontal cortex, amygdala, and hippocampus to coordinate emotions, memories, and impulses involved in eating and other rewarding behaviors. Previous research has demonstrated that insulin interacts with dopamine, altering activity of the mesocorticolimbic systems, inducing feelings of satiety and decreasing high-calorie food seeking. However, much of the existing research has been conducted in mice, using very high levels of insulin, making translation to humans difficult.
The investigators assigned ten male participants (average age, 27 years) with a normal BMI (average BMI, 24) to receive either intranasal insulin or a placebo and undergo a combined PET and MRI scan after having fasted overnight. The researchers gave participants an injection of a radioactive marker called [11C]-raclopride that binds to dopamine receptors so they could measure dopamine-related brain activity during the scan. Participants also completed surveys to assess eating behavior and provided a blood sample for measurement of insulin and other hormones.
Following administration of intranasal insulin, [11C]-raclopride synaptic binding potential increased in the ventral and dorsal striatum, suggesting an increase in the number of dopamine receptors in these regions. Accordingly, synaptic dopamine concentrations (dopamine that has not bound to a receptor and internalized by the neuron) decreased. Ultimately, this increase in dopamine signaling reduced resting-state activity in the ventral and dorsal striatum and improved functioning of mesocorticolimbic circuits 15 to 45 minutes after insulin exposure. As the participants' response to insulin exposure increased, so did their scores on tests of subjective wellbeing and cognitive control.
This study, which demonstrated the effects of intranasal insulin on dopamine activity in the mesocorticolimbic system, has important implications for reward-based learning, eating behavior, and obesity. Future research should include participants with insulin resistance to gain a better understanding of the effects of obesity and metabolic disease on the brain.
-
Stimulant medications increase willingness to expend effort, not ability. www.sciencedaily.com
Executive function refers to a set of cognitive abilities that facilitate control over voluntary behaviors, including attention control, working memory, and cognitive flexibility. While executive functions are critical for complex tasks such as planning, they are also mentally taxing. Without sufficient motivation, people with poor executive function may struggle to meet goals. Researchers report their findings that dopamine signaling is responsible for the effects of Ritalin and other stimulant medications on motivation and executive function.
Dopamine is one of the most abundant neurotransmitters in the brain and is involved in reward-motivated behavior, learning, and memory. Activities that provide a reward (e.g., food, money) increase dopamine levels, causing a sensation of pleasure that enhances learning by deeply encoding memories related to rewarding activities. Motivation to complete a task is based, in part, on whether a task is judged to provide sufficient pleasure relative to the cost of its required effort. Capacity to synthesize dopamine varies from person to person; however, lower dopamine levels in key brain areas are associated with attention deficit hyperactivity disorder (ADHD), substance use disorders, and Parkinson’s disease. Drugs such as methylphenidate (i.e., Ritalin), a medication used to treat ADHD, and sulpiride, a medication used to treat schizophrenia and depression, interact with dopamine receptors in the brain and can increase motivation.
The authors recruited 50 healthy adults (ages, 18 to 43 years). Participants completed a test called a cognitive effort-discounting paradigm. In this test, participants are asked how much money they would want to receive in exchange for completing tasks of varying difficulty. The authors measured the estimated effort cost as the amount of money necessary to make participants willing to perform a cognitively difficult working memory task. Participants completed effort-discounting tasks under the influence of 20 milligrams of methylphenidate, 400 milligrams of sulpiride, or a placebo on three separate testing days. The researchers used a positron emission tomography (PET) scan to measure dopamine synthesis capacity in the caudate nucleus, a brain region responsible for reward-based learning. Finally, the researchers used a statistical model based on the effort-discounting task to further explore the effects of methylphenidate and sulpiride on motivation.
While on the placebo treatment, participants’ willingness to expend cognitive effort increased as their baseline dopamine synthesis capacity increased. Notably, while performance on the working memory task decreased with difficulty, there was no relationship between task performance and dopamine levels. Both methylphenidate and sulpiride increased willingness to expend cognitive effort, but only in participants with low baseline dopamine synthesis capacity. Using their computer model, the investigators found that methylphenidate increased feelings of reward while sulpiride decreased effort cost. Further, they found that the cost-benefit analysis involved in the decision to expend effort occurs early in the decision-making process and can be measured by patterns in gaze (focusing on a reward or cost of a task) during cognitive testing. While higher baseline dopamine synthesis capacity and drug administration did not affect gaze patterns directy, higher dopamine levels strengthened the impact of gaze and attention to the benefits versus the costs of a decision.
These findings indicate that Ritalin and other attention-enhancing drugs work by increasing willingness to attempt cognitively-difficult tasks, not the ability.
-
People with Parkinson's disease that received a growth factor (GDNF) experienced a 100% improvement in dopamine uptake in a key brain region. sciencesources.eurekalert.org
People with Parkinson’s disease that received a growth factor (GDNF) experienced a 100% improvement in dopamine uptake in a key brain region involved in the disease compared to the placebo group which did not experience any change. The participants that received GDNF also showed moderate to large improvements in symptoms.
The GDNF was implanted into the brain using robot-assisted neurosurgery. This delivery system allowed a high flow rate of GDNF infusions that were administered every four weeks.
Parkinson’s disease leads to a substantial decrease in dopamine-producing neurons in the brain. These neurons are important for motor control and other cognitive functions.
Several animal studies have identified GDNF as an important regulator of dopamine neurons in the brain. Interestingly, animal studies have also shown that GDNF is produced in the brain after acute and long-term exercise. Exercise has been shown to improve Parkinson’s disease symptoms in several clinical trials.
-
UDP-glucuronosyltransferases (UGTs) of the blood-brain barrier: their role in drug metabolism and detoxication www.frontiersin.org
[Abstract]
UDP-glucuronosyltransferases (UGTs) form a multigenic family of membrane-bound enzymes expressed in various tissues, including brain. They catalyze the formation of β-D-glucuronides from structurally unrelated substances (drugs, other xenobiotics, as well as endogenous compounds) by the linkage of glucuronic acid from the high energy donor, UDP-α-D-glucuronic acid.
In brain, UGTs actively participate to the overall protection of the tissue against the intrusion of potentially harmful lipophilic substances that are metabolized as hydrophilic glucuronides. These metabolites are generally inactive, except for important pharmacologically glucuronides such as morphine-6-glucuronide. UGTs are mainly expressed in endothelial cells and astrocytes of the blood brain barrier (BBB). They are also associated to brain interfaces devoid of BBB, such as circumventricular organ, pineal gland, pituitary gland and neuro-olfactory tissues.
Beside their key-role as a detoxication barrier, UGTs play a role in the steady-state of endogenous compounds, like steroids or dopamine (DA) that participate to the function of the brain. UGT isoforms of family 1A, 2A, 2B and 3A are expressed in brain tissues to various levels and are known to present distinct but overlapping substrate specificity. The importance of these enzyme species with regard to the formation of toxic, pharmacologically or physiologically relevant glucuronides in the brain will be discussed.
-
Supplemental probiotics for 12 weeks improved cognition in Alzheimer's patients & also lowered inflammatory markers. www.sciencedaily.comBrain Alzheimer's Gut Microbiome Inflammation Probiotics Behavior Insulin Triglycerides Dopamine Norepinephrine Acetylcholine
The probiotics also lowered triglycerides, VLDL, and markers of insulin resistance. There was no cognitive improvement in the placebo group.
The participants took 2 billion Bifidobacterium bacteria per day, which is a pretty small quantity of probiotics. It is likely that the probiotics are working through multiple mechanisms such as lowering inflammation and increasing neurotransmitters. Other studies have shown that gut bacteria are able to modulate the levels of GABA, norepinephrine, serotonin, dopamine, and acetylcholine through the gut-brain axis.
I spoke with the gut experts, Drs. Justin and Erica Sonnenburg, about the importance of the gut microbiome in human health and the various foods (ie. fermentable fiber and other prebiotics) that provide our gut bacteria with the food they need to thrive. Here is the interview (also available on iTunes and Sticher): https://www.youtube.com/watch?v=gOZcbNw7sng