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The Big and Bangin' Pseudo-Advanced Drug Chemistry, Pharmacology and More Thread, V.2

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I'll admit I didn't read the article in any detail, I just used it to find a blood concentration associated with a dose range to answer your MAOI question.
 
Dr. Mind said:
New studies on neurological compounds have found that these new compounded chemicals can tap into an area of receptors damaged by drug or alcohol use, and slowly repair them to their normal state.
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What compounds are you referring to?
I've heard this same thing said of ketamine when used therapeutically and suspect MXE is capable of the same in the right amount.
Regarding MXE, on the last page of this thread I brought up MXE pharmacology and was interested in how it could increase dopamine levels even though it may not actually be a DRI or agonist directly. I was looking for evidence that the changes in glutamate function could cause changes in dopamine levels and, indeed, found this: http://apt.rcpsych.org/content/8/3/189.full " Thus, a reduced glutamate function, for example as induced by ketamine, may cause some elevation of dopamine release"
So there's that.
 
^^^^
The guy you were replying to was a bizarre spammer who was banned.
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But what indications do we have that these changes would be positive? I also suspect that the benefit doesn't extend to chronic usage, which at the very least lays outside the study's scope.

ebola
 
would 2mg of Prazosin (an α-antagonist) completely block the effects of amphetamines (300mg IV methamphetamine to be exact)? I take it for nightmares for PTSD, but thinking of dropping the med anyway and trying to get through them without it, but if the opportunity arises, "I dun wanna waste ma skrilla. Yanno wudda meen, monika?"
 
Hate to be that guy, but if you have nightmares from PTSD so terrible that you need medication then 300mg intravenous methamphetamine definitely isn't for you. It could make things much permanently worse.
 
^^^^^
He's essentially right.
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Unopposed beta agonism doesn't pose the same danger as unopposed alpha agonism (as the beta receptor exerts cardio effects similar to amp), so I think that you're okay, but your dose of meth is really high, and I'm not 100 percent confident in my info.

ebola
 
So, whats the deal with apigenin? It has a 0.2% BA from parsley but is supposed to be the active constituent in chamomile tea. It has a rich non selective pharmacology. GABA PAM and second order pam. It also has effects on adenosine and Serotonin reuptake.

What is also interesting about chamomile tea is that it has been shown to increase glycine levels in humans. Perhaps something in it is a glycine releaser?
 
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Is there any rule about how benzodiazepines changed to their thienodiazepine analogues (and the other way around) perform?

For example would the benzo version of etizolam retain activity:
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Or the thieno version of alprazolam:
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I'm just skeptical of the whole idea of a psychotomimetic. That a drug causes hallucinations and delusions does not suggest that it is qualitatively similar to organic psychosis, let alone any particular specific type thereof. Even the analogy between stimulant psychosis and paranoid schizophrenia is incomplete. And even if two states are qualitatively similar, this does not entail that they have similar biochemical bases.

In short, knowledge about one type of crazy rarely sheds light on another.

ebola
 
^ Great place to start though no? I mean you're right to be skeptical, drug induced psychosis never fully mimics schizophrenia. But studying psychotomimetic states allows us to tie a specific biochemical change to a psychotic state, then make predictions based on that association about causes/treatments for endogenous psychosis. When those predictions don't hold up it still informs what we know about those conditions, even though the model isn't perfecr.
 
endotropic said:
^ Great place to start though no? I mean you're right to be skeptical, drug induced psychosis never fully mimics schizophrenia. But studying psychotomimetic states allows us to tie a specific biochemical change to a psychotic state, then make predictions based on that association about causes/treatments for endogenous psychosis. When those predictions don't hold up it still informs what we know about those conditions, even though the model isn't perfecr.
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This.^ QFT
 
Yeah, but they used to use psychedelics to mimic schizophrenia and psychosis. We now know that psychedelia is very, very different from schizophrenia. Testing for psychotic symptoms on animals with any sort of hallucinogenic or proposed psychotomimetic is going to turn up looking pretty similar to schizophrenia, simply because a lot of their surface symptoms are similar. If one wants to understand schizophrenia using drugs, one must find a drug that acts uniquely both chemically, and on the subjective effects in humans. To test this again, a pharmacologically similar chemical should be tested. If they both have effects which in humans, in vivo, cause symptoms highly reminiscent of both the negative and positive effects of schizophrenia, then perhaps you have found how the disease works. Unless NMDA antagonist dissociatives all have highly schizophrenic-like symptoms, then perhaps you have found something. Unless MK801 or something very structurally similar exists in the human brain in schizophrenic patients, it is not very helpful.
 
DL-ark said:
Yeah, but they used to use psychedelics to mimic schizophrenia and psychosis. We now know that psychedelia is very, very different from schizophrenia. Testing for psychotic symptoms on animals with any sort of hallucinogenic or proposed psychotomimetic is going to turn up looking pretty similar to schizophrenia, simply because a lot of their surface symptoms are similar. If one wants to understand schizophrenia using drugs, one must find a drug that acts uniquely both chemically, and on the subjective effects in humans. To test this again, a pharmacologically similar chemical should be tested. If they both have effects which in humans, in vivo, cause symptoms highly reminiscent of both the negative and positive effects of schizophrenia, then perhaps you have found how the disease works. Unless NMDA antagonist dissociatives all have highly schizophrenic-like symptoms, then perhaps you have found something. Unless MK801 or something very structurally similar exists in the human brain in schizophrenic patients, it is not very helpful.
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I agree that intoxications with classical/serotonergic psychedelic is usually very unlike schizophrenia, but I have seen and experienced my fair share of psychedelics induced psychotic episodes (sometimes only for the duration of the intoxication) which strongly resemble paranoid schizophrenia to the last detail, both in people who turned out to be schizophrenic later in life and people who were never diagnosed with any psychotic illness. That being said, some dissociatives resemble schizophrenia a lot more I think, e.g. diphenidine and pcp come to mind.

Also it's probably noteworthy that when I had my first full-blown manic episode, I saw visuals that were subjectively identical to those I see on low dose tryptamines. However different all these states might be, they also bear some resemblance in many aspects.
 
crOOk said:
I agree that intoxications with classical/serotonergic psychedelic is usually very unlike schizophrenia, but I have seen and experienced my fair share of psychedelics induced psychotic episodes (sometimes only for the duration of the intoxication) which strongly resemble paranoid schizophrenia to the last detail, both in people who turned out to be schizophrenic later in life and people who were never diagnosed with any psychotic illness. That being said, some dissociatives resemble schizophrenia a lot more I think, e.g. diphenidine and pcp come to mind.

Also it's probably noteworthy that when I had my first full-blown manic episode, I saw visuals that were subjectively identical to those I see on low dose tryptamines. However different all these states might be, they also bear some resemblance in many aspects.
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All I am saying is that the purpose of using drugs to mimic schizophrenia is that if you make a drug, you will be able to know its pharmacology, and if it induces schizophrenesque psychosis without failure, then you can study its pharmacology and therefore learn the pharmacology of schizophrenia. Certain drugs causing psychotic episodes or full blown psychosis is not the same as this.
 
endo said:
Great place to start though no? I mean you're right to be skeptical, drug induced psychosis never fully mimics schizophrenia. But studying psychotomimetic states allows us to tie a specific biochemical change to a psychotic state, then make predictions based on that association about causes/treatments for endogenous psychosis.
Click to expand...

Right, this is useful, but at no point does it actually confirm the set of physiological processes underlying organic psychoses. Even with a properly psychotomimetic drug, we wouldn't gain a firm understanding of such, nor does the pharmacology of prevailing treatments provide a great deal of useful evidence. I hypothesize that the causal processes underlying organic psychosis occur at the ontological and epistemological level of neural circuits, so looking for a receptor or neurotransmitter that "mediates schizophrenia" is wrong-headed in the first place. However, this wouldn't preclude effective treatments rooted in drug-receptor interactions.

ebola
 
ebola? said:
Right, this is useful, but at no point does it actually confirm the set of physiological processes underlying organic psychoses. Even with a properly psychotomimetic drug, we wouldn't gain a firm understanding of such, nor does the pharmacology of prevailing treatments provide a great deal of useful evidence. I hypothesize that the causal processes underlying organic psychosis occur at the ontological and epistemological level of neural circuits, so looking for a receptor or neurotransmitter that "mediates schizophrenia" is wrong-headed in the first place. However, this wouldn't preclude effective treatments rooted in drug-receptor interactions.

ebola
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You are making valid points there and if you asked me the entire psychopharmacological field would be on the wrong track if it simply kept looking "for a receptor or neurotransmitter that" mediates any psychiatric illness. Your hypothesis is probably correct, at least I would agree, but I don't think that makes a case against the idea of using drug induced parapsychotic states to gain a better understanding of the processes involved in what we actually refer to as psychotic states.

We have a good concept of what "the ontological and epistemological level" consists of from a philosophical point of view, but there is very little (->no) understanding of the neurophysiological implications. Integrating these concepts into the picture should indeed be a long term goal and needless to say most neuroscientists will agree that a single proteine will not supply any answers. However at the current time our psychopharmaceuticals are simply at a very early, I dare say primitive stage and all we can really do is target select proteins and more often than not select actually means random ("look at what pushing this does, we didn't see that coming, did we?"). So for the time being, it might not be so bad to focus on this strategy for within-our-grasp treatment options which have already saved countless lives while still keeping in mind that we are actually not really on track in our quest to understand psychiatric illness.
 
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