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Dopamine receptors are a class of G protein-coupled receptors that are prominent in the vertebrate central nervous system (CNS) and are implicated in many neurological processes, including motivational and incentive salience, cognition, memory, learning, and fine motor control, as well as modulation of neuroendocrine signaling.
These drugs show greater magnitudes of impact on dopamine levels than do dopamine reuptake inhibitors like methylphenidate. [ 62 ] [ 63 ] In addition, whereas dopamine reuptake inhibitors show a clear dose–effect ceiling in their effects on dopamine levels, dopamine releasing agents do not and have been found to maximally increase dopamine ...
Dopamine agonists are often used in younger people as monotherapy and as initial therapy instead of L-DOPA. [7] Although it is important to know that there is a correlation between the two drugs, if l-DOPA doesn't work dopamine agonists are also ineffective. [1]
Clozapine is an example of a drug used in the treatment of certain CNS disorders, such as schizophrenia, that has superior efficacy precisely because of its broad-spectrum mode of action. Likewise, in cancer chemotherapeutics, it has been recognized that drugs active at more than one target have a higher probability of being efficacious.
Serotonin–dopamine releasing agents (SDRAs), for instance 5-chloro-αMT, are less common and are not selective for dopamine release, but have also been developed. [9] [14] Tryptamines like 5-chloro-αMT are the only known releaser scaffold that consistently release dopamine more potently than norepinephrine. [15]
This in turn leads to increased extracellular concentrations of both norepinephrine and dopamine and, therefore, an increase in adrenergic and dopaminergic neurotransmission. [1] A closely related type of drug is a norepinephrine–dopamine releasing agent (NDRA).
Drugs that increase dopamine in the brain, such as amphetamines, are known to cause psychosis, while drugs that treat psychosis do so by reducing dopamine activity.
A few endogenous MAEs have been identified, including the trace amines β-phenylethylamine (PEA), tyramine, and tryptamine. [1] [11] At a concentration of 16 μM (1.6 × 10-5 M), β-phenylethylamine has been shown to act as a MAE for norepinephrine (2.6-fold increase), dopamine (1.3-fold increase), and serotonin (2.3-fold increase) in the rat brainstem in vitro.
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