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Dopamine therapy is the regulation of levels of the neurotransmitter dopamine through the use of either agonists, or antagonists; and has been used in the treatment of disorders characterized by a dopamine imbalance. Dopamine replacement therapy (DRT) is an effective treatment for patients with decreased levels of dopamine.
Abnormal dopamine receptor signaling and dopaminergic nerve function is implicated in several neuropsychiatric disorders. [1] Dopamine receptors are therefore common drug targets. Dopamine receptors activate different effectors through not only G-protein coupling, but also signaling through different protein (dopamine receptor-interacting ...
It is unclear if dopamine is safe to use during pregnancy or breastfeeding. [4] At low doses dopamine mainly triggers dopamine receptors and β1-adrenergic receptors while at high doses it works via α-adrenergic receptors. [4] Dopamine was first synthesized in a laboratory in 1910 by George Barger and James Ewens in England. [8]
Dopamine receptor flow chart. Dopamine receptors are all G protein–coupled receptors, and are divided into two classes based on which G-protein they are coupled to. [1] The D 1-like class of dopamine receptors is coupled to Gα s/olf and stimulates adenylate cyclase production, whereas the D 2-like class is coupled to Gα i/o and thus inhibits adenylate cyclase production.
Dopamine (DA, a contraction of 3,4-dihydroxyphenethylamine) is a neuromodulatory molecule that plays several important roles in cells. It is an organic chemical of the catecholamine and phenethylamine families. Dopamine constitutes about 80% of the catecholamine content in the brain.
A dopamine agonist is a compound that activates dopamine receptors. There are two families of dopamine receptors, D 1-like and D 2-like. They are all G protein-coupled receptors. D 1 - and D 5-receptors belong to the D 1-like family and the D 2-like family includes D 2, D 3 and D 4 receptors. [1]
In animal models of depression, elevated activity has been reported in LHb neurons that project to the ventral tegmental area (ostensibly reducing dopamine release). The LHb also projects to aversion reactive mPFC neurons, which may provide an indirect mechanism for producing depressive behaviors. [ 134 ]
The risk factors [110] for treatment resistant depression are: the duration of the episode of depression, severity of the episode, if bipolar, lack of improvement in symptoms within the first couple of treatment weeks, anxious or avoidant and borderline comorbidity and old age. Treatment resistant depression is best handled with a combination ...