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The Large and Nifty Not-quite-advanced Drug Chemistry, Pharmacology and More Thread

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I made a BDD Dictionary, and I'd like to make sure some terms are properly defined. (Please keep in mind this is intended for a basic crowd;).)

NSFW:
Affinity- Force that impels certain atoms or molecules to bind to or unite with other atoms or molecules to form complexes or compounds; chemical attraction
Agonist- Drug that binds to a receptor in the brain, causing a chemical release
Antagonist- Drug that cancels the effect of an agonist, latches onto a receptor with greater efficiency
Anticholinergic- Drug that blocks Acetylcholine; works by competitive inhibition of ACh receptors in neurons
Bioavailability- A measure of the amount of drug that is actually absorbed from a given dose
Blood Brain Barrier- Naturally occurring barrier created by the modification of brain capillaries that prevents many substances from leaving the blood and crossing the capillary walls into the brain tissue

Ceiling- The maximum biological effect of a given drug, regardless of how large a dose is administered
Competitive Antagonist- Receptor antagonist that binds to a receptor but does not activate the receptor, will compete with available agonist for receptor binding sites on the same receptor
Cross-tolerance- Resistance to one or several effects of a drug as a result of tolerance developed to a pharmacologically similar compound

Efficacy- The capacity to produce an effect
Enantiomer- One of a pair of molecules that are nonsuperimposable mirror images of each other

First-Pass Metabolism- When a drug is administered orally, it passes through the liver before being absorbed
Latency period- Period of time which must elapse between when a dose of drug is taken and the time at which it produces effects
Ligand- Molecule that binds to a macromolecule, a ligand binding to a receptor

Metabolism- Sum of chemical and physical changes in tissue, chiefly of anabolism (those reactions that convert small molecules into large), and catabolism (those reactions that convert large molecules into small), including both endogenous large molecules as well as biodegradation
Neurotransmitter- Specific chemical released by a presynaptic cell that crosses the synapse to stimulate or inhibit the postsynaptic cell; neurotransmitters released by presynaptic cells may change transmitter release from presynaptic cells


Racemic- Mixture of an equal number of dextro- and levorotatory substances, which are separable
Receptor- Structural protein molecule on a cell's surface or within the cytoplasm that binds to a specific factor, such as a drug, hormone, antigen, or neurotransmitter

I hope this is ok :).
 
Two questions:
1. Would people be able to 'feel' in vivo whether something is a potent serotonergic neurotoxin, a la 4-chloro-amphetamine? I mean, MPTP's insta-Parkinsons is rather unmistakable. . .
2. Does anyone have info on interactions between tramadol and selegiline at maob-selective doses for the latter?

ebola
 
ebola? said:
Two questions:
1. Would people be able to 'feel' in vivo whether something is a potent serotonergic neurotoxin, a la 4-chloro-amphetamine? I mean, MPTP's insta-Parkinsons is rather unmistakable. . .
2. Does anyone have info on interactions between tramadol and selegiline at maob-selective doses for the latter?

ebola
Click to expand...

to 1.: This is rather improbable with regard to objective measurements. I mean, there are always certain people who think that they "feel" something in this respect, but I don't think that such effects are immediately feelable... Even MPTP (resp. MPP+) induced damage needs some time to develop (depending on the dose: ~days, I would think).

to 2.: To my best knowledge does a) tramadol not inhibit neither MAO-A nor -B and b) is not metabolized via any MAO. If the raised 5HT-levels pose a danger in combination with selegiline is a different question, which I'm not able to answer right now.

Peace! Murphy
 
Rocknroll-

Thanks again.



What does it mean if cabergoline does nothing to enhance one's libido? Could that mean that one had a highly developed prolactinoma? I've taken about 1.5 mgs this week and it has had only the vaguest positive impact upon my sex drive.

What are some possible pharmacological causes for hyperprolactinaemia? I've been taking docosahexaenoic acid and melatonin for months now and I'm beginning to suspect that they may be involved somehow. I know, for instance, that DHA somehow increases the activity of D1 receptors in the prefrontal cortex (perhaps it upregulates them?). If it had this effect on adenohypophyseal D1 receptors, it could very well produce a prolactinoma and thus hyperprolactinaemia. I say this by the following line of reasoning: I read a study which purported to show that cabergoline taken long-term (6 months or so) has the effect of shrinking prolactinomas - which result is retrograde to what intuition would suggest, which is that through homeostatic mechanisms the prolactinoma would become larger to compensate for decreased prolactin production and secretion. So if long-term D2 agonism can cause the shrinking of a prolactinoma then perhaps long-term D1 agonism can give rise to the hypertrophy of the portion of the adenohypophysis responsible for prolactin production.

P.S. I've noticed that when I quit DHA and go at least a month or thereabouts without it I notice positive changes in my range of emotions and my libido and that if, having quit for a month, I take just a single dose, I will perceive the onset of low libido and blunted emotions within an hour or two, which both last for at least a week thereafter.
 
I didn't know whether to post this here or is Science & Tech. I am doing some research into extracting morphine from poppy pods and have found a lot of interesting articles in journals on Google which I cannot access. How do I get access to these articles? Do I have to pay for every single article (which would cost a fortune) or can I pay a fixed fee so that I can get access to a large number of journals? I don't know anyone I can ask to access the journals for me on my behalf so I have to resort to paying :(
 
permastoned said:
Why do antihistamines that work centrally often (if not always?) tend to have anticholinergic effects?
Click to expand...

Sequence homology and/or structural similarity, I guess. I know very little about these things, but based on what I know, it seems that the only possible explanation is that antihistamines tend to antagonize the muscarinic acetylcholine receptors due to some similarity (not necessarily very great at all) between the geometry of the histamine and muscarinic acetylcholine receptors.

Mirtazapine, by the way, is one H1 antagonist that has negligible affinity for the muscarinic acetylcholine receptors.
 
Explain how Nitrous Oxide is a NMDA antagonist.

Does N2O affect any other receptors/neurotransmitters in the brain?

How is N2O metabolized?

Is there a dangerous number of 8g chargers not to go over in a single dose? I've done 3 at the most, but was thinking I may want to try 4. Essentially, what is the LD50?

Can you be allergic to N2O?
 
shibireru said:
Sequence homology and/or structural similarity, I guess. I know very little about these things, but based on what I know, it seems that the only possible explanation is that antihistamines tend to antagonize the muscarinic acetylcholine receptors due to some similarity (not necessarily very great at all) between the geometry of the histamine and muscarinic acetylcholine receptors.

Mirtazapine, by the way, is one H1 antagonist that has negligible affinity for the muscarinic acetylcholine receptors.
Click to expand...

That's what I figured. Just it seems that nobody ever points it out or uses data to prove it. I cant do all that computer combinatorial chem or whatever, 3d drug design. Histamine and acetylcholine look quite different to me. But as I said, without the 3d I cant really tell. Dont know how to compare the receptors without a wiki picture either.. and it hasn't been made for the muscarinics.
 
Bob Loblaw said:
I made a BDD Dictionary, and I'd like to make sure some terms are properly defined. (Please keep in mind this is intended for a basic crowd;).)

NSFW:
Affinity- Force that impels certain atoms or molecules to bind to or unite with other atoms or molecules to form complexes or compounds; chemical attraction
Agonist- Drug that binds to a receptor in the brain, causing a chemical release
Antagonist- Drug that cancels the effect of an agonist, latches onto a receptor with greater efficiency
Anticholinergic- Drug that blocks Acetylcholine; works by competitive inhibition of ACh receptors in neurons
Bioavailability- A measure of the amount of drug that is actually absorbed from a given dose
Blood Brain Barrier- Naturally occurring barrier created by the modification of brain capillaries that prevents many substances from leaving the blood and crossing the capillary walls into the brain tissue

Ceiling- The maximum biological effect of a given drug, regardless of how large a dose is administered
Competitive Antagonist- Receptor antagonist that binds to a receptor but does not activate the receptor, will compete with available agonist for receptor binding sites on the same receptor
Cross-tolerance- Resistance to one or several effects of a drug as a result of tolerance developed to a pharmacologically similar compound

Efficacy- The capacity to produce an effect
Enantiomer- One of a pair of molecules that are nonsuperimposable mirror images of each other

First-Pass Metabolism- When a drug is administered orally, it passes through the liver before being absorbed
Latency period- Period of time which must elapse between when a dose of drug is taken and the time at which it produces effects
Ligand- Molecule that binds to a macromolecule, a ligand binding to a receptor

Metabolism- Sum of chemical and physical changes in tissue, chiefly of anabolism (those reactions that convert small molecules into large), and catabolism (those reactions that convert large molecules into small), including both endogenous large molecules as well as biodegradation
Neurotransmitter- Specific chemical released by a presynaptic cell that crosses the synapse to stimulate or inhibit the postsynaptic cell; neurotransmitters released by presynaptic cells may change transmitter release from presynaptic cells


Racemic- Mixture of an equal number of dextro- and levorotatory substances, which are separable
Receptor- Structural protein molecule on a cell's surface or within the cytoplasm that binds to a specific factor, such as a drug, hormone, antigen, or neurotransmitter

I hope this is ok :).
Click to expand...

I'm just going to bump this :).
 
Bob Loblaw said:
I'm just going to bump this :).
Click to expand...

A few changes I would recommend.

An agonist does not always cause a chemical release. Rather, you can say that it will initiate a cascade of reactions within the target cell. Additionally, I hate to be picky, but it is not always a drug, by saying this you completely disregard endogenous agonists. Additionally, it is not always in the brain

Agonist: Compound that binds to a receptor, activating it and initiating a cascade of reactions within the receptor's cell.

Change drug in antagonist to compound aswell. Your definition of antagonist is actually a competitive antagonist. An antagonist does not have to latch onto the cell with greater efficiency, all an antagonist needs to be an antagonist is to bind to, but not activate the receptor.

as such

Antagonist: Compound that binds to a receptor, but does not activate it.

Then you have competitive antagonist later which is correct

Last thing

First-pass metabolism.. this is incorrect. It can not pass through the liver before being absorbed, I think you mean that after it is absorbed, it passes through the liver before it can reach other tissues in the body (hepatic portal vein).

However, you must realise that second-pass metabolism also occurs in the liver.

A simple way to desribe it (this is as simple as I can make it without killing myself, I hate excluding info. you cut parts out yourself):

The aim of metabolism is to convert fat soluble drugs into water soluble substances that can be excreted by the kidneys;

First-pass metabolism occurs after absorption of the drug from the stomach or intestine, where it flows directly through the hepatic portal vein to the liver. The effect is to alter the drug to reveal or create a new functional group, an example being an oxidation reaction. This occurs in the smooth endoplasmic reticulum of the liver.

Second-pass metabolism, which occurs in the cytosol of the liver, attaches the new functional group to an endogenous water soluble substance, which will allow the drug to be excreted by the kidneys. An example is glucronidation.




Take what you want from my suggestions :)
 
Just making sure I have my information correct:

The new theory for tolerance (at least for opioids) is that the receptor density increases, and that the G-proteins uncouple from the receptors, right?
 
super potent phenethylamine vasoconstriction

the bromo-dfly wikipedia states:

"Also, a Swedish man had to have the front part of his feet and several fingers on one hand amputated after taking a massive overdose. Apparently the compound acted as a long-acting efficacious vasoconstrictor, leading to necrosis and gangrene which was delayed by several weeks after the overdose occurred. Several other cases have also been reported of severe peripheral vasoconstriction following overdose with Bromo-DragonFLY, and a similar case is also known from DOB"



is this true?



and why?
 
i dont know for sure, but one time on a high dosage of dob my legs felt painful as hell.

For some reason after i quit smoking the "painfulness" of this drug did not occur although its still a powerful vasopressor and hypertension may be an issue (if u take too much).
 
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