I'm hijacking this thread.
In response to Toast[us] from the thread "Receptor Effects",
Don't forget about Apigenin. I'm a little confused with when you said "by the lack of the dopamine transporter". I thought it was an activator. And oh apparently Apigenin acts on the benzo receptors (Can you clear up what the difference is between the GABA and benzo receptors?), so maybe I can take this in the afternoon way before luteolin. Whatcha think?
Luteolin activates the dopamine transporter. By doing this it causes the dopamine transporter to downregulate. After it wears off you feel a dopamine build up, similar but not identical to cocaine. But dopamine reuptake inhibitors feed dopamine into the nausea center, so the downregulation induced by luteolin will do the same thing. If you want to experience euphoria after the luteolin wears off you'll need to use a 5-HT3 antagonist to block the nausea.
Apigenin is, to my knowledge, an NMDA antagonist and a Benzodiazepine-receptor Positive Allosteric Modulator. The Benzodiazepine receptor is this little spot on the GABA-A receptor that is different from other spots on the receptor that other molecules bind to. Benzo's like this little spot better than the other spots for some reason. Apigenin should cause sedation by potentiating this receptor.
I don't see a connection between apigenin and luteolin. What idea did you have about combining them?
Alibaba offers Luteolin. What about that?
If you can order anything from alibaba, do it. I'm still trying to learn how to use it.
Both Apigenin and Luteolin have very low oral bioavailability. What can I take to increase that? Some type of oil or cytochrome inhibitor?
Luteolin is very active in me at 50 mg. Doesn't feel like it has low bioavailability to me. I wouldn't want it any stronger. I've never tried apigenin before, though I have had effects from a gram of parsley [mild dissociation].
Oh, I just read that article, and it says apigenin is also a mild DA/NE reuptake enhancer but less potent than luteolin. Nice. I still don't know why I would use it with luteolin though.
contradicts ur previous statement with lobelia. How blocking monoamine transporters will result in upregulation. The article says at the end, activations results in upregulation and this other article (which I've showed you before):
Shows a downregulation with the blockage of DAT transporters. Explain yourself Toast!!!
"I've read about tianeptine, the serotonin reuptake enhancer. Would be nice, but I don't think I could get it, I don't know how to order from offshore pharmacies or alibaba.com yet. I'm trying to learn how to order from alibaba so I can get some amentoflavone for 5-HT2C antagonism. All the herbs that have amentoflavone screw up its effects and make it get metabolized in like 2 minutes so you barely feel it. I'd like to use inhibitors with it, like ginger."
I don't see a contradiction with anything I said.
"Thus, luteolin and apigenin function as monoamine transporter
activators, which would improve several hypermonoaminergic
neuropsychological disorders, especially cocaine dependence, through
up-regulating monoamine transporter activity."
By upregulating, they mean the action of luteolin on the transporter, not the reaction the body produces in response to luteolin's presence. Luteolin boosts the transporter, causing the body to downregulate it. If you don't believe me, try it yourself. I suspect this is just a jargon-based misunderstanding. Upregulating probably means several things to them, like the action of luteolin is to upregulate the transporter while it is in the system. I know for a fact, from personal experience, that luteolin downregulates the transporter after it leaves the body. I know what it feels like and I can differentiate it from placebo. I also know that luteolin causes this by activating the transporter because I can feel it. Taking luteolin sucks but its worth it.
"Three months after initiation of treatment with methylphenidate we found
a down-regulation of the post-synaptic dopamine receptor with a maximum
of 20 % and a down-regulation of the dopamine transporter with a
maximum of 74.7 % in the striatal system."
Oh, this is interesting. How would that work... A reuptake inhibitor causing reverse tolerance... In my experience all reuptake inhibitors cause upregulation of the transporter. I've never felt reverse tolerance, not even to methylphenidate. That would be interesting to try, but I don't want to risk my transporters, lol.
Now, it is possible that my understanding of lobelia is not correct, and that VMAT is the only transporter needed to be inhibited. Regardless, inhibition of both transporters by lobelia results in an upregulation of some type that feels like a natural amphetamine-state. It may be due purely to the VMAT, since we know upregulation of the dopamine transporter reduces synaptic dopamine and therefore sucks.
I suspect the good effect is due to VMAT upregulation, allowing each neuron to fire more transmitter per action potential. I don't know how much it is dependent on an increased supply of cytoplasmic dopamine caused by the increase in the dopamine transporter.
Doesn't amentoflavone promote alzheimers developement via inhibition of cathepsin B?
That would suck. I guess I'll have to take my chances, lol. 5-HT2C antagonism is something you HAVE to experience. It's like pure magic.