The reduction in presynaptic dopamine release produced by tyrosine and phenylalanine depletion offers the potential to lower the activity of dopamine pathways through a novel mechanism. Such an action could produce beneficial effects for a variety of neuropsychiatric syndromes in which clinical symptoms have been linked to increased dopamine release, such as acute schizophrenia and mania.
Dopamine - Serotonin's Secret Weapon A smart dopamine med may do wonders for your depression or mania or psychosis or mental acuity. The problem is one does not exist. by John McManamy For two years running, dopamine has received my Newsletter’s coveted "Neurotransmitter of the Year" award.
This key neurotransmitter is also required for social function, and low levels can result in social anxiety, phobias, and depression, whereas excess levels can be associated with bipolar disorder and mania. (9, 10, 11)
The early oral dopamine agonists were ergot derivatives acting primarily on the D 2-like (D 2, D 3 and D 4) dopamine receptors (although pergolide has weak D 1 agonist activity and bromocriptine has D 1 antagonist activity). Examples of this type of dopamine agonist are bromocriptine, pergolide, lisuride, and the long acting ergoline, cabergoline.
C. Cariprazine (Vraylar) is FDA-approved for schizophrenia and mania, and it also has positive placebo-controlled data in bipolar depression and as an adjunct to antidepressants in unipolar depression. It differs from the others in that it is more potent at dopamine D3 receptors than at D2 receptors.
Excess dopamine receptors and a hyperactive reward process network may underly the manic phase of the condition. Meanwhile, decreases in levels of a substance called dopamine transporter may contribute to lower dopamine function and depression. The overall problem may be with dopamine regulation, not simply highs or lows.
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