3 replies to this topic

[Pike]

i'm noticing how all of these expensive prolactin inhibitors are all coincidentally dopamine agonists. then i discover that, lo and behold, dopamine in and of itself is a prolactin inhibitor. then, i found out that the Prolactin Inhibiting Hormone (PIH) was actually just another synonym of dopamine.

http://www.ncbi.nlm....pubmed/11739329

Dopamine is a small and relatively simple molecule that fulfills diverse functions. Within the brain, it acts as a classical neurotransmitter whose attenuation or overactivity can result in disorders such as Parkinson's disease and schizophrenia. Major advances in the cloning and characterization of biosynthetic enzymes, transporters, and receptors have increased our knowledge regarding the metabolism, release, reuptake, and mechanism of action of dopamine. Dopamine reaches the pituitary via hypophysial portal blood from several hypothalamic nerve tracts that are regulated by PRL itself, estrogens, and several neuropeptides and neurotransmitters. Dopamine binds to type-2 dopamine receptors that are functionally linked to membrane channels and G proteins and suppresses the high intrinsic secretory activity of the pituitary lactotrophs. In addition to inhibiting PRL release by controlling calcium fluxes, dopamine activates several interacting intracellular signaling pathways and suppresses PRL gene expression and lactotroph proliferation. Thus, PRL homeostasis should be viewed in the context of a fine balance between the action of dopamine as an inhibitor and the many hypothalamic, systemic, and local factors acting as stimulators, none of which has yet emerged as a primary PRL releasing factor. The generation of transgenic animals with overexpressed or mutated genes expanded our understanding of dopamine-PRL interactions and the physiological consequences of their perturbations. PRL release in humans, which differs in many respects from that in laboratory animals, is affected by several drugs used in clinical practice. Hyperprolactinemia is a major neuroendocrine-related cause of reproductive disturbances in both men and women. The treatment of hyperprolactinemia has greatly benefited from the generation of progressively more effective and selective dopaminergic drugs.

so who's going to keep on buying their bromocriptine and cabergoline now?

[bran319]

So, what exactly is your point?

[FunkOdyssey]

i'm noticing how all of these expensive prolactin inhibitors are all coincidentally dopamine agonists. then i discover that, lo and behold, dopamine in and of itself is a prolactin inhibitor. then, i found out that the Prolactin Inhibiting Hormone (PIH) was actually just another synonym of dopamine.

http://www.ncbi.nlm....pubmed/11739329

Dopamine is a small and relatively simple molecule that fulfills diverse functions. Within the brain, it acts as a classical neurotransmitter whose attenuation or overactivity can result in disorders such as Parkinson's disease and schizophrenia. Major advances in the cloning and characterization of biosynthetic enzymes, transporters, and receptors have increased our knowledge regarding the metabolism, release, reuptake, and mechanism of action of dopamine. Dopamine reaches the pituitary via hypophysial portal blood from several hypothalamic nerve tracts that are regulated by PRL itself, estrogens, and several neuropeptides and neurotransmitters. Dopamine binds to type-2 dopamine receptors that are functionally linked to membrane channels and G proteins and suppresses the high intrinsic secretory activity of the pituitary lactotrophs. In addition to inhibiting PRL release by controlling calcium fluxes, dopamine activates several interacting intracellular signaling pathways and suppresses PRL gene expression and lactotroph proliferation. Thus, PRL homeostasis should be viewed in the context of a fine balance between the action of dopamine as an inhibitor and the many hypothalamic, systemic, and local factors acting as stimulators, none of which has yet emerged as a primary PRL releasing factor. The generation of transgenic animals with overexpressed or mutated genes expanded our understanding of dopamine-PRL interactions and the physiological consequences of their perturbations. PRL release in humans, which differs in many respects from that in laboratory animals, is affected by several drugs used in clinical practice. Hyperprolactinemia is a major neuroendocrine-related cause of reproductive disturbances in both men and women. The treatment of hyperprolactinemia has greatly benefited from the generation of progressively more effective and selective dopaminergic drugs.

so who's going to keep on buying their bromocriptine and cabergoline now?

Everyone already knew this. The dopamine agonists inhibit prolactin more thoroughly than physiological dopamine can, producing effects like the drastic reduction or near elimination of the male refractory period as an example...

[acantelopepope]

So, what exactly is your point?

I second that.


I haven't taken any prolactin inhibitors, but if I were to, it would be to increase dopamine, because (as far as I knew) it was in the realm of common knowledge that dopamine and prolactin share an antagonistic relationship.

Interesting example: after ejaculation, the male's dopamine drops as prolactin increases, explaining the "pulling away" phenomenon.

See this for more information: http://www.entelechy..._after_sex1.htm

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