5-HT1a agonism decreases ejaculation latency in male rats
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I was reviewing some of the many studies on lisuride when I came across this one:
So the underlying mechanism, or at least one of them, behind lisuride's effects are NOT due to dopamine agonism, as lisuride exhibited the same effects when when the dopamine receptors were blocked by a stronger antagonist. Or, to put it another way, although dopamine might have positive effects, lisuride does not rely on them solely.
I also found this study:
Specific involvement of central 5-HT1A receptors in the mediation of male rat ejaculatory behavior
It appears as though the underlying mechanism to facilitate rat sexual behavior COULD be agonism of the 5-HT1a serotonin receptor. Now, this is where I'm confused. The horrible SSRIs that nobody Peating is a fan of indirectly agonize this and other serotonin receptors. How is it possible to agonize these same receptors by blocking the pathways to deplete serotonin, much like how lisuride is a general serotonin agonist (with the notable exception of 5-HT2b), yet yield the opposite behavior, PSSD?
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@engineer Agonism of the serotonin 1a receptor, causes a negative feedback loop. reducing serotonin
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@engineer Zinc, bromocriptine increases / agnoises 5-HT1a
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@alfredoolivas So why don't SSRIs do the same because they agonize 5-HT1a too?
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@engineer They increase prolactin via inhbiting serotonin reuptake.
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@alfredoolivas Let's say SSRIs +serotonin -> +prolactin. And because lisuride +dopamine -> -prolactin while +5-HT1a, the rats exhibit their plucky behavior. Are you saying that the reason SSRIs are so bad is because they force serotonin to increase, even though the 5-HT1a receptors are screaming "less serotonin" meanwhile serotonin continues to build up, leading to overload in the other receptors?
I am just super curious about this stuff because it is unbelievably more complicated than even photonics engineering
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@engineer as you know it's a lot more complicated than a single receptor (5-HT2C is also involved) and it's more complicated than receptors, because SSRIs would increase other biomolecules such as prolactin, AcTH or adrenaline, that also impact sexual function.
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@engineer AcTH can give erections by binding to the melanocortin 2 receptors, just like melanotan I,II or PT 141. So fascinating how this "pituarity hormone" works on the family of receptors that alpha msh / sun hormones work on.
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SSRIs have a much more generalized effect than a direct 5-HT1a receptor agonist since serotonin will be divided among all other receptors
From another study
