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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 ...
Other dopaminergic drugs that have been used or suggested in the treatment of disorders of diminished motivation include rasagiline (a selective monoamine oxidase B (MAO-B) inhibitor; but see more below), tolcapone (a centrally-acting catechol-O-methyltransferase (COMT) inhibitor), and amantadine (an indirectly acting dopaminergic agent that ...
Amantadine has dopaminergic effects through uncertain mechanisms of action. [24] [25] It is structurally related to other adamantanes like bromantane and rimantadine, which also have dopaminergic actions. [26] Bromantane can upregulate tyrosine hydroxylase (TH) and thereby increase dopamine production and this might be involved in its ...
Central dopaminergic agonist properties of semisynthetic ergoline derivatives lergotrile, pergolide, bromocriptine and lisuride have been established. Some studies suggest that ergot alkaloids have the properties of mixed agonist-antagonist with regards to certain presynaptic and postsynaptic receptors.
Lack of dopamine reuptake and the increase in extracellular levels of dopamine have been linked to increased susceptibility to addictive behavior given increase in dopaminergic neurotransmission. [citation needed] The dopaminergic pathways are considered to be strong reward centers.
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.
The mechanisms of sympathomimetic drugs can be direct-acting (direct interaction between drug and receptor), such as α-adrenergic agonists, β-adrenergic agonists, and dopaminergic agonists; or indirect-acting (interaction not between drug and receptor), such as MAOIs, COMT inhibitors, release stimulants, and reuptake inhibitors that increase the levels of endogenous catecholamines.
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).