The Affect of Sequence when Ingesting Multiple Different Drugs?

[Theconfusedstoner]

Hi, this is my first post on Bluelight, so let me know if I'm doing something wrong! I have searched the internet far and wide and have found little to no information on the affect that sequencing has when taking multiple different drugs at the same time. I'm no expert, and correct me if I'm wrong, but when a drug is taken, chemicals called neurotransmitters are released from the drug, and attach to specific receptors in the brain. When these receptors are activated by the drugs neurotransmitter, the neurotransmitter attaches to the receptor site which tells the brain to release dopamine or serotonin or whatever. Now, here's my question. Say you take, "drug A" which affects a certain amount of receptors in the brain, and then an hour later, you take, "drug B" which affects some of the, but not all of the, same receptors. Would some of the neurotransmitters from drug B not be able to affect the same receptors that drug A had already affected? Would sequencing in drugs have any affect at all? With my minimal knowledge of pharmacology, it seems like sequencing would have a major role when taking multiple drugs at once! Neurotransmitters and their receptor sites were always explained with the, "Key in a lock" metaphor, implying that there is only one neurotransmitter for each receptor site, and only one neurotransmitter can be in a receptor at a time. It seems to me like one drug could produce neurotransmitters that may overlap/affect the neurotransmitters of another drug that is taken simultaneously. So if anybody has an answer, or can describe to me the affect of sequencing in layman's terms, it would be appreciated!

 

[sekio]

but when a drug is taken, chemicals called neurotransmitters are released from the drug, and attach to specific receptors in the brain. When these receptors are activated by the drugs neurotransmitter, the neurotransmitter attaches to the receptor site which tells the brain to release dopamine or serotonin or whatever.

This is not quite what occurs. Neurotransmitters aren't released from a drug: the drug acts in lieu of the neurotransmitter, and only certain classes of drugs produce massive release of other neurotransmitters.

Some drugs produce their effects by binding directly to receptors and either activating them (full or partial agonists) or preventing them from being activated (antagonists). These receptors produce downstream effects in cells like casuing them to signal, or to inhibit releasing a chemical, or whatever. This is the mode of action of stuff like LSD, opioids, GHB etc.

Some drugs produce their effects by binding to other targets, like e.g. monoamine transporters, and thereby interfere with the normal processing of monoamines to increase their concentrations in certain areas. (SSRIs, cocaine, methylphenidate) Some drugs go a step further and reverse the monoamine transporters causing monoamine release (MDMA, amphetamines).

To answer your question, it depends on the particular drug in question and how much of it you're taking. Sometimes one drug will block anothers effects because it has higher affinity (bonds more tightly) to a common receptor - buprenorphine & other opioids is a common scenario.

Human biology is really tricky.

 

[Trying2Iso]

It is important to be distinct when referring to "releasing agents" or "reuptake inhibitors" they are different in function

 

[Theconfusedstoner]

Thanks, this was very informative! But when you refer to bupe as having a higher affinity, are you referring to how some people will take bupe, and go into withdrawl? Because i thought that some kinds of bupe are mixed with another drug, (anavar, or something like that) that is meant to be an opiate agonist, which immediately knocks off all opiates from their receptors, and this is why some users will have a shit ton of opiates in there system, and then take bupe, expecting to get high, but instead just get some nasty withdrawl symptoms.

 

[sekio]

Buprenorphine has a higher affinity for opioid receptors than naloxone does. But even pure bupre will cause precipitated withdrawals: it's only a partial agonist and other opioids are more weakly binding full agonists.

 

[serotonin2A]

Thanks, this was very informative! But when you refer to bupe as having a higher affinity, are you referring to how some people will take bupe, and go into withdrawl? Because i thought that some kinds of bupe are mixed with another drug, (anavar, or something like that) that is meant to be an opiate agonist, which immediately knocks off all opiates from their receptors, and this is why some users will have a shit ton of opiates in there system, and then take bupe, expecting to get high, but instead just get some nasty withdrawl symptoms.

The high affinity of buprenorphine isn't so much the issue here, rather it is the fact that it is a partial agonist (meaning that it produces a submaximal amount of receptor activation). Someone who is dependent on a full agonist will require a certain level of receptor activation at all times to prevent withdrawal, but if buprenorphine displaces some of the full agonist, there will be a net reduction in receptor activation. The high affinity of buprenorphine isn't necessarily relevant, because even low affinity ligands can displace high affinity ligands when present at sufficiently high concentration.

 

[Researchers]

There’s a book called buzzed it’s all the Info you need to know from alcohol to xanax. It was like my guide as a teen so I knew effects of mixing certain drugs also considering I have a seizure disorder I gotta be weary

 

[Researchers]

I love your technical response

 

[busted.produk]

There’s a book called buzzed it’s all the Info you need to know from alcohol to xanax.

I remember that book...
It was givin to me back in high school(20 years ago)...
While it does have some info, its more like the "cliff notes" version of "a dummies guide to...."
Im sure theyve updated it from my version throughout the years though...

Kudos on your thirst for knowledge OP