37 replies to this topic

[Nattzor]

 

So, I understand that PRL 8-53 is a dopamine agonist, along with its Histamine 3 inverse agonism and a host of other unknown MoAs. Now, it was mentioned that it potentiates the dopaminergic effects of other substances. However, it was also mentioned that PRL 8-53 *does not* potentiate the effects of amphetamines, but it only mentioned that in relation to its actions on serotonin and norepinephrine, ignoring dopamine altogether. Now, you can certainly tell where this is going, and why I labeled it as a "stupid" question. So, being that dopamine was not mentioned with regards to potentiation, I extrapolated that the dopaminergic effects of amphetamines are in fact potentiated by this substance, but without having seen this confirmed in the paper, I cant say definitively if this is true. Now, this may have been mentioned in the full study, but I only have access to the abstract and what I recall of the many PRL-related discussions on the web, here on Longecity as well as over on Reddit and a host of other sources, so that's what I'm basing my understanding on at the moment. Now, it's a bit embarrassing that I'd even be asking this, but I'm certainly far from a pharmacologist, just an individual with a strong curiosity for a plethora of topics, pharmacology/neurology-related or otherwise. Blame the Aspergers, haha. Now, I assume I'm right on this point, but there's certainly a chance I could be wrong. So, just for the sake of confirmation: correct or incorrect?

 

To update, after doing some more research on this topic, I've determined that my initial thoughts were correct. 3AlarmLampScooter mentioned that amphetamines and PRL-8-53 synergize well, which I've found to be the case as well. Indeed, the dopaminergic effects do seem to be potentiated with this combination. It's not definitive proof, and it is somewhat subjective, but it's good enough for me.

 

 

Where did you get the Histamine 3 inverse agonist from and the norepinephrine from? The paper does not talk about that at all. And afaik, they tested amphetamines and PRL and it did not potentiate, so they didn't just say it from a theoretical view.

[serp777]

 

So, I understand that PRL 8-53 is a dopamine agonist, along with its Histamine 3 inverse agonism and a host of other unknown MoAs. Now, it was mentioned that it potentiates the dopaminergic effects of other substances. However, it was also mentioned that PRL 8-53 *does not* potentiate the effects of amphetamines, but it only mentioned that in relation to its actions on serotonin and norepinephrine, ignoring dopamine altogether. Now, you can certainly tell where this is going, and why I labeled it as a "stupid" question. So, being that dopamine was not mentioned with regards to potentiation, I extrapolated that the dopaminergic effects of amphetamines are in fact potentiated by this substance, but without having seen this confirmed in the paper, I cant say definitively if this is true. Now, this may have been mentioned in the full study, but I only have access to the abstract and what I recall of the many PRL-related discussions on the web, here on Longecity as well as over on Reddit and a host of other sources, so that's what I'm basing my understanding on at the moment. Now, it's a bit embarrassing that I'd even be asking this, but I'm certainly far from a pharmacologist, just an individual with a strong curiosity for a plethora of topics, pharmacology/neurology-related or otherwise. Blame the Aspergers, haha. Now, I assume I'm right on this point, but there's certainly a chance I could be wrong. So, just for the sake of confirmation: correct or incorrect?

 

To update, after doing some more research on this topic, I've determined that my initial thoughts were correct. 3AlarmLampScooter mentioned that amphetamines and PRL-8-53 synergize well, which I've found to be the case as well. Indeed, the dopaminergic effects do seem to be potentiated with this combination. It's not definitive proof, and it is somewhat subjective, but it's good enough for me.

 

It seems like a bad combination. It could lead to over stimulation of neurons and therefore cell death. Seems really risky to be trying combinations of nootropics with a compound that barely has any scientific evidence supporting it. Amphetamines also have questionable long term effects. It's plausible that negative long term side effects synergize as well. 

[Ekscentra]

 

 

So, I understand that PRL 8-53 is a dopamine agonist, along with its Histamine 3 inverse agonism and a host of other unknown MoAs. Now, it was mentioned that it potentiates the dopaminergic effects of other substances. However, it was also mentioned that PRL 8-53 *does not* potentiate the effects of amphetamines, but it only mentioned that in relation to its actions on serotonin and norepinephrine, ignoring dopamine altogether. Now, you can certainly tell where this is going, and why I labeled it as a "stupid" question. So, being that dopamine was not mentioned with regards to potentiation, I extrapolated that the dopaminergic effects of amphetamines are in fact potentiated by this substance, but without having seen this confirmed in the paper, I cant say definitively if this is true. Now, this may have been mentioned in the full study, but I only have access to the abstract and what I recall of the many PRL-related discussions on the web, here on Longecity as well as over on Reddit and a host of other sources, so that's what I'm basing my understanding on at the moment. Now, it's a bit embarrassing that I'd even be asking this, but I'm certainly far from a pharmacologist, just an individual with a strong curiosity for a plethora of topics, pharmacology/neurology-related or otherwise. Blame the Aspergers, haha. Now, I assume I'm right on this point, but there's certainly a chance I could be wrong. So, just for the sake of confirmation: correct or incorrect?

 

To update, after doing some more research on this topic, I've determined that my initial thoughts were correct. 3AlarmLampScooter mentioned that amphetamines and PRL-8-53 synergize well, which I've found to be the case as well. Indeed, the dopaminergic effects do seem to be potentiated with this combination. It's not definitive proof, and it is somewhat subjective, but it's good enough for me.

 

 

Where did you get the Histamine 3 inverse agonist from and the norepinephrine from? The paper does not talk about that at all. And afaik, they tested amphetamines and PRL and it did not potentiate, so they didn't just say it from a theoretical view.

 

 

The H3 inverse agonism came from an anecdote, and not too reliable of one, in fact. It seems I was mistaken there. Post #1531 in the original PRL-8-53 thread was the one that mentioned this MoA.

 

The paper did in fact mention norepinephrine and serotonin not being potentiated, but failed to mention dopamine. In my most recent personal experiences, PRL-8-53 displays an additive dopaminergic effect, not a true synergy as I had originally thought.

[Ekscentra]

 

 

So, I understand that PRL 8-53 is a dopamine agonist, along with its Histamine 3 inverse agonism and a host of other unknown MoAs. Now, it was mentioned that it potentiates the dopaminergic effects of other substances. However, it was also mentioned that PRL 8-53 *does not* potentiate the effects of amphetamines, but it only mentioned that in relation to its actions on serotonin and norepinephrine, ignoring dopamine altogether. Now, you can certainly tell where this is going, and why I labeled it as a "stupid" question. So, being that dopamine was not mentioned with regards to potentiation, I extrapolated that the dopaminergic effects of amphetamines are in fact potentiated by this substance, but without having seen this confirmed in the paper, I cant say definitively if this is true. Now, this may have been mentioned in the full study, but I only have access to the abstract and what I recall of the many PRL-related discussions on the web, here on Longecity as well as over on Reddit and a host of other sources, so that's what I'm basing my understanding on at the moment. Now, it's a bit embarrassing that I'd even be asking this, but I'm certainly far from a pharmacologist, just an individual with a strong curiosity for a plethora of topics, pharmacology/neurology-related or otherwise. Blame the Aspergers, haha. Now, I assume I'm right on this point, but there's certainly a chance I could be wrong. So, just for the sake of confirmation: correct or incorrect?

 

To update, after doing some more research on this topic, I've determined that my initial thoughts were correct. 3AlarmLampScooter mentioned that amphetamines and PRL-8-53 synergize well, which I've found to be the case as well. Indeed, the dopaminergic effects do seem to be potentiated with this combination. It's not definitive proof, and it is somewhat subjective, but it's good enough for me.

 

It seems like a bad combination. It could lead to over stimulation of neurons and therefore cell death. Seems really risky to be trying combinations of nootropics with a compound that barely has any scientific evidence supporting it. Amphetamines also have questionable long term effects. It's plausible that negative long term side effects synergize as well. 

 

 

It's a legitimate concern, but if my most recent (subjective) thoughts are correct, then keeping the doses low and dosing very infrequently should mitigate this. I didn't choose this combo expecting any safety guarantees, but the benefits have outweighed the risks for me, and so I'll continue to use this combo on occasion until I run into anything worrying, at which point I'll back off and stick to one of the two substances alone, or perhaps nothing at all. Right now, I don't have any evidence pointing to any real danger in this combination, and I need the concentration and focus more than ever. I can't function or get any work done without stimulants, period. I'll keep that in mind regardless, and if it comes down to it, I'll discontinue promptly. I'm not claiming this combination is safe by any means, and I wouldn't suggest anyone else attempt this, but in my case, it's a whole lot better than the alternative.

[Nattzor]

 

 

 

So, I understand that PRL 8-53 is a dopamine agonist, along with its Histamine 3 inverse agonism and a host of other unknown MoAs. Now, it was mentioned that it potentiates the dopaminergic effects of other substances. However, it was also mentioned that PRL 8-53 *does not* potentiate the effects of amphetamines, but it only mentioned that in relation to its actions on serotonin and norepinephrine, ignoring dopamine altogether. Now, you can certainly tell where this is going, and why I labeled it as a "stupid" question. So, being that dopamine was not mentioned with regards to potentiation, I extrapolated that the dopaminergic effects of amphetamines are in fact potentiated by this substance, but without having seen this confirmed in the paper, I cant say definitively if this is true. Now, this may have been mentioned in the full study, but I only have access to the abstract and what I recall of the many PRL-related discussions on the web, here on Longecity as well as over on Reddit and a host of other sources, so that's what I'm basing my understanding on at the moment. Now, it's a bit embarrassing that I'd even be asking this, but I'm certainly far from a pharmacologist, just an individual with a strong curiosity for a plethora of topics, pharmacology/neurology-related or otherwise. Blame the Aspergers, haha. Now, I assume I'm right on this point, but there's certainly a chance I could be wrong. So, just for the sake of confirmation: correct or incorrect?

 

To update, after doing some more research on this topic, I've determined that my initial thoughts were correct. 3AlarmLampScooter mentioned that amphetamines and PRL-8-53 synergize well, which I've found to be the case as well. Indeed, the dopaminergic effects do seem to be potentiated with this combination. It's not definitive proof, and it is somewhat subjective, but it's good enough for me.

 

 

Where did you get the Histamine 3 inverse agonist from and the norepinephrine from? The paper does not talk about that at all. And afaik, they tested amphetamines and PRL and it did not potentiate, so they didn't just say it from a theoretical view.

 

 

The H3 inverse agonism came from an anecdote, and not too reliable of one, in fact. It seems I was mistaken there. Post #1531 in the original PRL-8-53 thread was the one that mentioned this MoA.

 

The paper did in fact mention norepinephrine and serotonin not being potentiated, but failed to mention dopamine. In my most recent personal experiences, PRL-8-53 displays an additive dopaminergic effect, not a true synergy as I had originally thought.

 

 

H3 inverse agonist was when isochroma confused it for another compound (and iirc, tried to mock me for not "knowing" it was a H3 inverse agonist). I still don't see norepinephrine in the paper, can you give me the quote? It only talks about dopaminergic, serotoninergic and cholinergic systems afaik.

 

http://www.reddit.co...s/1d40a5/prl853

[Ekscentra]

 

 

 

 

So, I understand that PRL 8-53 is a dopamine agonist, along with its Histamine 3 inverse agonism and a host of other unknown MoAs. Now, it was mentioned that it potentiates the dopaminergic effects of other substances. However, it was also mentioned that PRL 8-53 *does not* potentiate the effects of amphetamines, but it only mentioned that in relation to its actions on serotonin and norepinephrine, ignoring dopamine altogether. Now, you can certainly tell where this is going, and why I labeled it as a "stupid" question. So, being that dopamine was not mentioned with regards to potentiation, I extrapolated that the dopaminergic effects of amphetamines are in fact potentiated by this substance, but without having seen this confirmed in the paper, I cant say definitively if this is true. Now, this may have been mentioned in the full study, but I only have access to the abstract and what I recall of the many PRL-related discussions on the web, here on Longecity as well as over on Reddit and a host of other sources, so that's what I'm basing my understanding on at the moment. Now, it's a bit embarrassing that I'd even be asking this, but I'm certainly far from a pharmacologist, just an individual with a strong curiosity for a plethora of topics, pharmacology/neurology-related or otherwise. Blame the Aspergers, haha. Now, I assume I'm right on this point, but there's certainly a chance I could be wrong. So, just for the sake of confirmation: correct or incorrect?

 

To update, after doing some more research on this topic, I've determined that my initial thoughts were correct. 3AlarmLampScooter mentioned that amphetamines and PRL-8-53 synergize well, which I've found to be the case as well. Indeed, the dopaminergic effects do seem to be potentiated with this combination. It's not definitive proof, and it is somewhat subjective, but it's good enough for me.

 

 

Where did you get the Histamine 3 inverse agonist from and the norepinephrine from? The paper does not talk about that at all. And afaik, they tested amphetamines and PRL and it did not potentiate, so they didn't just say it from a theoretical view.

 

 

The H3 inverse agonism came from an anecdote, and not too reliable of one, in fact. It seems I was mistaken there. Post #1531 in the original PRL-8-53 thread was the one that mentioned this MoA.

 

The paper did in fact mention norepinephrine and serotonin not being potentiated, but failed to mention dopamine. In my most recent personal experiences, PRL-8-53 displays an additive dopaminergic effect, not a true synergy as I had originally thought.

 

 

H3 inverse agonist was when isochroma confused it for another compound (and iirc, tried to mock me for not "knowing" it was a H3 inverse agonist). I still don't see norepinephrine in the paper, can you give me the quote? It only talks about dopaminergic, serotoninergic and cholinergic systems afaik.

 

http://www.reddit.co...s/1d40a5/prl853

 

Yes, that was the instance I was referring to. Originally, I had thought that came from a legitimate study. Well, that was certainly one of the more blatant information mix-ups going around on these boards, I'd say!

 

As for the paper, we seem to be referring to two entirely different papers here, as there was another one that mentioned norepinephrine. I'll see if I can find it at some point. As far as I'm aware, it was a full paper, not an abstract, and it had included various tables comparing results in memory improvement. That's all I can recall at the moment.

[Nattzor]

 

 

 

 

H3 inverse agonist was when isochroma confused it for another compound (and iirc, tried to mock me for not "knowing" it was a H3 inverse agonist). I still don't see norepinephrine in the paper, can you give me the quote? It only talks about dopaminergic, serotoninergic and cholinergic systems afaik.

 

http://www.reddit.co...s/1d40a5/prl853

 

Yes, that was the instance I was referring to. Originally, I had thought that came from a legitimate study. Well, that was certainly one of the more blatant information mix-ups going around on these boards, I'd say!

 

As for the paper, we seem to be referring to two entirely different papers here, as there was another one that mentioned norepinephrine. I'll see if I can find it at some point. As far as I'm aware, it was a full paper, not an abstract, and it had included various tables comparing results in memory improvement. That's all I can recall at the moment.

 

 

That's not the paper, just a write-up I did on what I found out about PRL. I guess you'll find the study here: www.longecity.org/forum/topic/57942-plr-8-147-the-most-powerful-memory-enhancer/page__st__660#entry578884 (referenced in the bottom of the write-up), it has the tables you're talking about (also linked as images in the write-up). I might have missed it when reading, please correct me if I'm wrong.

 

http://examine.com/s...ments/PRL-8-53/ - Seems like I was wrong, it was the other study that talked about epi. Totally missed it when I wrote the write-up because I assumed it was only in German.

Here it is:

http://i.imgur.com/ZXGX1Sg.png

http://i.imgur.com/7D3JJiA.png

[Ekscentra]

 

 

 

 

 

H3 inverse agonist was when isochroma confused it for another compound (and iirc, tried to mock me for not "knowing" it was a H3 inverse agonist). I still don't see norepinephrine in the paper, can you give me the quote? It only talks about dopaminergic, serotoninergic and cholinergic systems afaik.

 

http://www.reddit.co...s/1d40a5/prl853

 

Yes, that was the instance I was referring to. Originally, I had thought that came from a legitimate study. Well, that was certainly one of the more blatant information mix-ups going around on these boards, I'd say!

 

As for the paper, we seem to be referring to two entirely different papers here, as there was another one that mentioned norepinephrine. I'll see if I can find it at some point. As far as I'm aware, it was a full paper, not an abstract, and it had included various tables comparing results in memory improvement. That's all I can recall at the moment.

 

 

That's not the paper, just a write-up I did on what I found out about PRL. I guess you'll find the study here: www.longecity.org/forum/topic/57942-plr-8-147-the-most-powerful-memory-enhancer/page__st__660#entry578884 (referenced in the bottom of the write-up), it has the tables you're talking about (also linked as images in the write-up). I might have missed it when reading, please correct me if I'm wrong.

 

http://examine.com/s...ments/PRL-8-53/ - Seems like I was wrong, it was the other study that talked about epi. Totally missed it when I wrote the write-up because I assumed it was only in German.

Here it is:

http://i.imgur.com/ZXGX1Sg.png

http://i.imgur.com/7D3JJiA.png

 

Yes, that's the one. Excellent work!