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Dopamine
Dr. Dawn-Elise Snipes, PhD
Executive Director, AllCEUs Counselor Education
Host: Counselor Toolbox Podcast

Objectives
~ What is it and what is itā€™s function?
~ How does it interact with serotonin, norepinephrine and GABA?
~ What are symptoms of excess?
~ How do you decrease it?
~ What are symptoms of insufficiency?
~ How do you increase it?
What is it and what is itā€™s function?

~ Neurotransmitter located throughout the body including the brain immune system, the kidneys and the pancreas.
~ Dopamine does not cross the bloodā€“brain barrier, so its synthesis and functions in peripheral areas are to a large degree independent of its synthesis and functions in the brain
~ Synthesized from L-Dopa
~ Is the main motivation/pleasure chemical ā€œmotivational salienceā€
~ Reduces insulin production (increase food intake) which impacts serotonin levels

What is it and what is itā€™s function?

~ Reduces gastrointestinal motility and protects intestinal mucosa
~ Reduces the activity of lymphocytes
~ Mood
~ Coordination and muscle movements
~ Learning, attention & memory (prefrontal cortex)
~ Regulates the flow of information from other areas of the brain (problem solving) (Frontal lobe and thalamus)
~ Wakefulness (people with Parkinsonā€™s or on antipsychotics are often sleepy)

Subtypes of Dopamine Receptors
~ D1
~ Most abundant dopamine receptor in the central nervous system
~ Regulate neuronal growth and development, mediate some behavioral responses
~ Agonists
~ Parkinsonā€™s medications

Receptors
~ D1
~ Agonists
~ Terguride:
~ Treatment for hyperprolactinemia (hypoestrogenism)/PCOS and treatment of pulmonary arterial hypertension
~ Serotonin receptor antagonist (5-HT2B, 5HT2A)
~ 5-HT2A receptor antagonists interfere with the heightened state of dopamine activity, and may be useful in the treatment of psychosis, and alcohol and cocaine dependence.
~ 5-HT2B antagonists have previously been proposed as treatment for migraine headaches and heart disease
~ Dopamine receptor agonist

Subtypes of Dopamine Receptors
~ D2
~ Schizophrenia can be attributed to an imbalance in dopaminergic pathways that signal D2 and D1 receptors
~ Most antipsychotics are antagonists for the dopamine D2 receptor
~ Parkinsonā€™s disease (PD) is an extrapyramidal motor disorder characterized by dopaminergic neuronal degeneration, esp. D2
~ Rewarding food stimulates dopaminergic transmission especially to the D2 receptor suggesting that dopamine deficiency in obese individuals may perpetuate pathological eating as a means to compensate for decreased activation
~ MDD patients showed decreased dopamine in the central and basal nuclei of the amygdala of postmortem depressed patients who committed suicide compared with control subjects

Subtypes of Dopamine Receptors
~ D1 receptors ‘prepare' the set of possible appropriate responses.
~ D2-shape and ‘select' from this initial response set framework
Dopamine and Depression
~ 2/3 of patients are not achieving remission with current SSRI medications
~ Anhedonia contributes to the persistence of MDD
~ Depression and anhedonia have been shown to be associated with a reduced striatal (dopamine)response to reward
~ Most antidepressant treatments do not directly enhance dopamine, which may contribute to residual symptoms, including impaired motivation, concentration, and pleasure
~ Tricyclic Antidepressants and MAOIs increase serotonin, norepinephrine and dopamine but have significant side effects

Dopamine and Depression
~ Latest generation of antidepressants
~ Norepinephrine and Dopamine reuptake inhibitors (bupropion/Wellbutrin)
~ Dopamine can decrease inflammation
~ Dopamine excess may cause vitamin B6 deficiency

Dopamine and Anxiety
~ Both dopamine D1 and D2 receptor mechanisms are important in mediating anxiety
~ Dopamine antagonists, have been reported to be associated with SAnD symptoms in patients treated for Touretteā€™s syndrome and schizophrenia.
~ Patients with SAnD are commonly treated with serotonergic antidepressants, however interplay with dopaminergic systems is understood to occur and the clinical effects of these agents may be mediated by processes such asD2 receptor sensitization
~ The most convincing evidence for reduced DA function in humans has been shown in SPECT neuroimaging studies

Dopamine and Addiction
~ Genetic differences that alter the expression of dopamine receptors in the brain can predict whether a person will find stimulants appealing or aversive
~ Consumption of stimulants produces increases in brain dopamine levels that last from minutes to hours.
~ Chronic elevation in dopamine triggers a wide-ranging set of structural changes in the brain that are responsible for the behavioral abnormalities which characterize an addiction.
How Does It Interact
~ Play a role in depression, along with the other neurotransmitters serotonin and norepinephrine
~ Dopaminergic system is modulated by several neurotransmitters, including glutamatergic neurons, GABAergic fibers
~ Changes in the glutamatergic, and GABAergic, and dopaminergic system may influence anxiety-likeor depressive behavior
~ Dopamine inhibits norepinephrine (get up and go)

How Does It Interact
~ Dopamine vs. Serotonin
~ Dopamine system dysfunction is linked to certain symptoms of depression, such as low motivation.
~ Serotonin is involved in how you process your emotions, which can affect your overall mood.
~ Both are involved in sleep, inflammation, appetite and energy levels

Symptoms of Dopamine Insufficiency
~ Muscle cramps, spasms, or tremors
~ Aches and pains
~ Restless legs
~ ADHD
~ Loss of balance
~ Constipation
~ Difficulty eating and swallowing
~ Trouble sleeping or disturbed sleep
~ Low energy
~ An inability to focus
~ Moving or speaking more slowly than usual
~ Feeling demotivated, hopeless
~ Feeling inexplicably sad or tearful
~ Mood swings
~ Feeling hopeless
~ Suicidal thoughts or thoughts of self-harm
~ Low sex drive
~ Loss of coordination (i.e. Parkinsonā€™s disease)

What Increases It
~ Cocaine, amphetamines (including methamphetamine), nicotine, ADHD medications, MDMA (ecstasy) and other psychostimulants.
~ Medications for Parkinsonā€™s and RLS
~ Opioids
~ Dopamine reuptake inhibitors (methylphenidate)
~ Decrease sugar and caffeine to reduce dopamine flooding (Chromium can help with sugar cravings and depression)
~ Get sufficient quality sleep and set circadian rhythms
~ Exercise increases hormones that increase dopamine
~ Decrease stress

What Increases It
~ L-Phenylalanine ā†’ L-Tyrosine ā†’ L-DOPA ā†’ Dopamine
~ Aspartame is made by joining together the amino acids aspartic acid and phenylalanine
~ The consumption of aspartame, unlike dietary protein, can elevate the levels of phenylalanine and aspartic acid in the brain. These compounds can inhibit the synthesis and release of neurotransmitters, dopamine, norepinephrine, and serotonin, which are known regulators of neurophysiological activity.
~ Increase tyrosine by eating bananas, almonds, apples, watermelons, cherries, yogurt, beans, eggs and meats (Tyrosine can cross the BBB)
~ Supplements to boost levels of vitamin D, magnesium, and omega-3 essential fatty acids may also help to raise dopamine levels
~ Address magnesium/zinc imbalances

What Increases It
~ Green Tea
~ Ginkgo
~ SAM-e
~ Ginseng
~ Kava
~ Clary sage, bergamot, lavender, lemon and rosemary essential oils
~ inhalation of essential oils can communicate signals to the olfactory system and stimulate the brain to exert neurotransmitters (e.g. serotonin and dopamine) thereby further regulating mood.ā€
How do Essential Oils Work
~ When tiny molecules of essential oils are dissolved in the nose it stimulates olfactory receptors, which activates cells that carry signals from the essential oil scent to other areas in the limbic system; the primal brain responsible for memory, instinct and mood.
~ The olfactory system is the only sensory mechanism that involves the limbic system and amygdala in its primary processing pathway.
~ This also explains why scents are the strongest triggers for memory.

Symptoms of Excess
~ Tics
~Hallucinations

~Delusions
~ Hypersexuality
~ Mania
~ Paranoia
~ Constipation

How to Decrease It
~ Most antipsychotic drugs are dopamine antagonists
~ Antinausea drugs
~ Tricyclic antidepressants (increase serotonin and reduce dopamine)
~ Melatonin is regulated by norepinephrine
~ Dopamine inhibits the effects of norepinephrine — which means a decrease in the production and release of melatonin
Summary
~ What is it and what is itā€™s function?
~ Pleasure and motivation
~ How does it interact with serotonin, norepinephrine and GABA?
~ What are symptoms of excess?
~ Psychosis, Tics
~ How do you decrease it?
~ Antipsychotics
~ What are symptoms of insufficiency?
~ Parkinsonā€™s, depression, anxiety, difficulty problem solving
~ How do you increase it?
~ Diet, exercise, sleep, some essential oils, NDRIs