Buprenorphine is more than just an opioid

[someguyontheinternet]

Here are excerpts from the studies:

*Diphenhydramine's GABA-B Receptor Agonism (2018)*

European Journal of Pharmacology, Volume 834, 2018

"...Diphenhydramine exhibited potent GABA-B receptor agonist activity, with an EC50 value of 34.6 ± 4.2 nM... The efficacy of diphenhydramine at the GABA-B receptor was 60-80% of the maximum response... These findings suggest that diphenhydramine's sedative and anxiolytic effects may be mediated, at least in part, by its GABA-B receptor agonist activity."

*Phenobarbital's GABA-B Receptor Agonism (2020)*

Neuropharmacology, Volume 168, 2020

"...Phenobarbital displayed high affinity for the GABA-B receptor, with a Ki value of 12.1 ± 1.5 nM... Phenobarbital acted as a full agonist at the GABA-B receptor, inducing a maximal response... The results indicate that phenobarbital's sedative, hypnotic, and anticonvulsant effects are likely mediated by its potent GABA-B receptor agonism."

Could you please point to the exact papers you're referencing? I can't seem to locate them

Here are the issues that you're citing, the papers should be on these pages

https://www.sciencedirect.com/journal/european-journal-of-pharmacology/vol/834/suppl/C

Neuropharmacology | Vol 168, 15 May 2020 | ScienceDirect.com by Elsevier

Read the latest articles of Neuropharmacology at ScienceDirect.com, Elsevier’s leading platform of peer-reviewed scholarly literature

www.sciencedirect.com

 

[Skorpio]

Here are excerpts from the studies:

*Diphenhydramine's GABA-B Receptor Agonism (2018)*

European Journal of Pharmacology, Volume 834, 2018

"...Diphenhydramine exhibited potent GABA-B receptor agonist activity, with an EC50 value of 34.6 ± 4.2 nM... The efficacy of diphenhydramine at the GABA-B receptor was 60-80% of the maximum response... These findings suggest that diphenhydramine's sedative and anxiolytic effects may be mediated, at least in part, by its GABA-B receptor agonist activity."

*Phenobarbital's GABA-B Receptor Agonism (2020)*

Neuropharmacology, Volume 168, 2020

"...Phenobarbital displayed high affinity for the GABA-B receptor, with a Ki value of 12.1 ± 1.5 nM... Phenobarbital acted as a full agonist at the GABA-B receptor, inducing a maximal response... The results indicate that phenobarbital's sedative, hypnotic, and anticonvulsant effects are likely mediated by its potent GABA-B receptor agonism."

These papers don’t exist.

Please stop using LLMs without checking the validity of the output. They will create papers telling you exactly what you want to see, but they are purely a hallucination.

This misinformation squarely flies in the face of bluelight’s mission of harm reduction.

 

[DeathIndustrial88]

This post feels completely littered with misinformation.


200mg of benadryl is 1-2mg of xanax???? Wtf. Not even remotely accurate.

Buprenorphine a stronger NMDA antagonist than DXM? Give me a break. I've been on bupe for 8 years & I use to use DXM to lower my tolerance to bupe. Pretty sure buprenorphine has literally ZERO NDMA properties. If it did, it would LOWER your tolerance to other opioids, but instead it can actually HEIGHTEN your tolerance to the lower-level potency opioids (like codeine, tramadol, hydrocodone, etc..).


I DO believe buprenorphine affects serotonin in some shape or form. Because I get moderate serotonin syndrome by mixing bupe + SSRIs...
Here's my sources - https://pubmed.ncbi.nlm.nih.gov/18774063/

But the HOW & WHY are missing. Because as far as I know, buprenorphine doesn't bind to anything serotonin-related. So I'd love to know why this happens.

Tramadol is an incredibly weak TAAR1 agonist & NMDA antagonist. Being weak doesn't mean it's not relevant, I'm a big fan of tramadol, I was hooked on it for 11 years before I got on bupe, but this also isn't new information. Tramadol is one of my favorite opioids next to heroin because it gives that light serotonin-releasing feeling, almost like you took a small dose of meth with your opioid or something.


Diphenhydramine (benadryl) is an antihistamine & anticholinergic drug, definitely not a substitute for any gaba-related dependencies.

 

[The Holy Quadruplty]

H1 receptor antagonists that cross the blood brain barrier do the exact opposite of what you are claiming, they decrease the activity of glutamine synthetase which is an enzyme involved in the production of GABA. This means that it actually LOWERS GABA and INCREASES the seizure threshold.

Chronic h1-antihistamine treatment increases seizure susceptibility after withdrawal by impairing glutamine synthetase - PubMed

Chronic H1-antihistamine treatment produces long-lasting increase in seizure susceptibility in nonepileptic rodents after drug withdrawal and its mechanism involves impairment of GS through blocking the action of histamine.

pubmed.ncbi.nlm.nih.gov

are you serious? you say you're writing a book, essentially on the pharmacology of these substances yet you don't even have a grasp of the basics? you don't know what the gamma subunit of the GABA receptor is? this must be a joke
the gamma subunit of the GABAa receptor is specific to the synaptic form of the receptor and it is essential for forming the benzodiazepine binding site



you don't have a grasp on the things you're writing about and you refuse to cite any sources besides meta AI. quite frankly your book is going to be filled with absolute nonsense, falsehoods, and misinformation and nobody will take it seriously. I think I've tried being nice about this but your continual refusal to even go over basic published research shows that you don't care about the accuracy of your information

Yea I do. I also have information yiu can't find on Google about this stuff, just wait you'll see. Humbly/Respectfully.

 

[The Holy Quadruplty]

By the way this is off topic, but has anyone here ever tried flunitrazepam, and if so did it taste similar to Xanax at all?

What other LONG ACTING Benzodiazepines/Triazolobenzodiazepines taste simular to Xanax, as I'm trying to figure something out?

 

[The Holy Quadruplty]

Could you please point to the exact papers you're referencing? I can't seem to locate them

Here are the issues that you're citing, the papers should be on these pages

https://www.sciencedirect.com/journal/european-journal-of-pharmacology/vol/834/suppl/C

Neuropharmacology | Vol 168, 15 May 2020 | ScienceDirect.com by Elsevier

Read the latest articles of Neuropharmacology at ScienceDirect.com, Elsevier’s leading platform of peer-reviewed scholarly literature

www.sciencedirect.com

Just gave you that for now since I'm going to be putting the sources in my books. I'll try to send you like a couple more I guess here shortly if i dont forget, but I'm not trying to give out too many for free when I'm about to be making money doing it shortly/humbly. Lol

 

[The Holy Quadruplty]

This post feels completely littered with misinformation.


200mg of benadryl is 1-2mg of xanax???? Wtf. Not even remotely accurate.

Buprenorphine a stronger NMDA antagonist than DXM? Give me a break. I've been on bupe for 8 years & I use to use DXM to lower my tolerance to bupe. Pretty sure buprenorphine has literally ZERO NDMA properties. If it did, it would LOWER your tolerance to other opioids, but instead it can actually HEIGHTEN your tolerance to the lower-level potency opioids (like codeine, tramadol, hydrocodone, etc..).


I DO believe buprenorphine affects serotonin in some shape or form. Because I get moderate serotonin syndrome by mixing bupe + SSRIs...
Here's my sources - https://pubmed.ncbi.nlm.nih.gov/18774063/

But the HOW & WHY are missing. Because as far as I know, buprenorphine doesn't bind to anything serotonin-related. So I'd love to know why this happens.

Tramadol is an incredibly weak TAAR1 agonist & NMDA antagonist. Being weak doesn't mean it's not relevant, I'm a big fan of tramadol, I was hooked on it for 11 years before I got on bupe, but this also isn't new information. Tramadol is one of my favorite opioids next to heroin because it gives that light serotonin-releasing feeling, almost like you took a small dose of meth with your opioid or something.


Diphenhydramine (benadryl) is an antihistamine & anticholinergic drug, definitely not a substitute for any gaba-related dependencies.

You're definitely going to want to read my books then...

 

[The Holy Quadruplty]

Spoiler: this post contains false information generated by LLMs

This post feels completely littered with misinformation.


200mg of benadryl is 1-2mg of xanax???? Wtf. Not even remotely accurate.

Buprenorphine a stronger NMDA antagonist than DXM? Give me a break. I've been on bupe for 8 years & I use to use DXM to lower my tolerance to bupe. Pretty sure buprenorphine has literally ZERO NDMA properties. If it did, it would LOWER your tolerance to other opioids, but instead it can actually HEIGHTEN your tolerance to the lower-level potency opioids (like codeine, tramadol, hydrocodone, etc..).


I DO believe buprenorphine affects serotonin in some shape or form. Because I get moderate serotonin syndrome by mixing bupe + SSRIs...
Here's my sources - https://pubmed.ncbi.nlm.nih.gov/18774063/

But the HOW & WHY are missing. Because as far as I know, buprenorphine doesn't bind to anything serotonin-related. So I'd love to know why this happens.

Tramadol is an incredibly weak TAAR1 agonist & NMDA antagonist. Being weak doesn't mean it's not relevant, I'm a big fan of tramadol, I was hooked on it for 11 years before I got on bupe, but this also isn't new information. Tramadol is one of my favorite opioids next to heroin because it gives that light serotonin-releasing feeling, almost like you took a small dose of meth with your opioid or something.


Diphenhydramine (benadryl) is an antihistamine & anticholinergic drug, definitely not a substitute for any gaba-related dependencies.

Here are some sources comparing the NMDA antagonist effects of Buprenorphine and Ketamine:

_Study 1:_

"Buprenorphine: A Unique Opioid Receptor Partial Agonist with NMDA Antagonist Properties" (2017)

Journal of Pharmacology and Experimental Therapeutics, Volume 362, Issue 2.

"...Buprenorphine exhibited potent NMDA receptor antagonism, with an IC50 value of 1.4 ± 0.3 μM... In comparison, ketamine's IC50 value was 4.8 ± 1.1 μM."

_Study 2:_

"Comparative Analysis of NMDA Receptor Antagonism by Opioids and Other Drugs" (2020)

European Journal of Pharmacology, Volume 866.

"...Buprenorphine demonstrated stronger NMDA receptor antagonism than ketamine... Buprenorphine's Ki value was 0.62 ± 0.12 μM, whereas ketamine's Ki value was 1.8 ± 0.4 μM."

_Study 3:_

"NMDA Receptor Antagonism by Buprenorphine and Its Relationship to Clinical Efficacy" (2019)

Journal of Clinical Psychopharmacology, Volume 39, Issue 3.

"...Buprenorphine's NMDA receptor antagonism was significantly more potent than ketamine's... The study suggests that buprenorphine's unique pharmacological profile may contribute to its therapeutic effects."

Here are some sources on GABA-A effects by Diphenhydramine:

*Journal Articles:*

1. "Diphenhydramine's GABA-A Receptor Agonist Activity" (2015)
Journal of Pharmacology and Experimental Therapeutics, Vol. 355, Issue 2.
DOI: 10.1124/jpet.115.226331

2. "GABA-A Receptor Modulation by Diphenhydramine" (2018)
European Journal of Pharmacology, Vol. 834.
DOI: 10.1016/j.ejphar.2018.02.014

3. "Diphenhydramine's Sedative Effects: Involvement of GABA-A Receptors" (2020)
Receptor Ag

 

[someguyontheinternet]

Here are some sources comparing the NMDA antagonist effects of Buprenorphine and Ketamine:

_Study 1:_

"Buprenorphine: A Unique Opioid Receptor Partial Agonist with NMDA Antagonist Properties" (2017)

Journal of Pharmacology and Experimental Therapeutics, Volume 362, Issue 2.

"...Buprenorphine exhibited potent NMDA receptor antagonism, with an IC50 value of 1.4 ± 0.3 μM... In comparison, ketamine's IC50 value was 4.8 ± 1.1 μM."

_Study 2:_

"Comparative Analysis of NMDA Receptor Antagonism by Opioids and Other Drugs" (2020)

European Journal of Pharmacology, Volume 866.

"...Buprenorphine demonstrated stronger NMDA receptor antagonism than ketamine... Buprenorphine's Ki value was 0.62 ± 0.12 μM, whereas ketamine's Ki value was 1.8 ± 0.4 μM."

_Study 3:_

"NMDA Receptor Antagonism by Buprenorphine and Its Relationship to Clinical Efficacy" (2019)

Journal of Clinical Psychopharmacology, Volume 39, Issue 3.

"...Buprenorphine's NMDA receptor antagonism was significantly more potent than ketamine's... The study suggests that buprenorphine's unique pharmacological profile may contribute to its therapeutic effects."

Here are some sources on GABA-A effects by Diphenhydramine:

*Journal Articles:*

1. "Diphenhydramine's GABA-A Receptor Agonist Activity" (2015)
Journal of Pharmacology and Experimental Therapeutics, Vol. 355, Issue 2.
DOI: 10.1124/jpet.115.226331

2. "GABA-A Receptor Modulation by Diphenhydramine" (2018)
European Journal of Pharmacology, Vol. 834.
DOI: 10.1016/j.ejphar.2018.02.014

3. "Diphenhydramine's Sedative Effects: Involvement of GABA-A Receptors" (2020)
Receptor Ag

Your DOIs are incorrect

The first does not exist and the second leads to a completely different paper

You have repeatedly ignored multiple people who tried to warn you that what you are posting is not real yet you continue to misrepresent the text output of large language models.

https://www.sciencedirect.com/science/article/abs/pii/S001429991830089X?via%3Dihub

 

[deficiT]

Bad thread is bad. Night folks.