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Opioids opioids effect (specifically oxycodone) on dopamine, norepinephrine, serotonin, etc

enoughorangejuice?

Bluelighter
Joined
Jan 7, 2007
Messages
3,213
I was just wondering why oxycodone particularly, and all opioids, even though classified as narcotics or depressants/downers provide many people with an increase in alertness, productivity and mental energy (at certain doses).

Is this because opioids affect dopamine and norepinephrine as well as the mu- and kappa-opioid receptors?

Basically I noticed that when I take opioids at a normal dose (not so high that i'm nodding) I am able to concentrate/read/focus better and it relieves any ADD/ADHD symptoms. I am more productive, reading/writing is easier. CNS stimulants like methylphenidate, amphetamines and caffeine also provide these effects so I was curious as to whether opioids and stimulants share some of the same neurotransmitters that they affect.

:sus:
Thanks!
 
Opioids increase levels of prefrontal cortex Dopamine, relieving ADD much in the same manner as amphetamines do.

The difference is that opioids release the DA indirectly through a strange mechanism, rather than directly as with amphetamines. Then, the dopamine that is released by opioids is eventually broken down in to norepinephrine, which is partly responsible for the typical opiate-induced insomnia. Natural and semi-synthetic opiates don't have any appreciable affinity for 5-HT receptors.

People find opioids to be as good of an ADD medication as amps, and don't realize that combining a normally used ADD dosage of amphetamines with their opioids causes their low pf cortex DA levels to increase twofold, pushing it higher than the intended normal transmitting levels (normally focused), in to abusive, euphoric pf DA levels, causing focus and short term memory to once again deteriorate. If you are taking opioids, you will need a much lower dosage of amphetamines than non-opioid users would need to treat ADD. Combining the two increases the risk of amphetamine neurotoxicity through dopamine autoxidation, as dopamine is dopamine to the brain; it doesn't matter if it is increased by opioids or amphetamines.

Keep in mind that the purposes of ADD medications are simply to increase focus and alertness. The side effects of forced motivation, euphoria, anorexia, insomnia, anxiety, restlessness, neurotoxicity, and hyperfocus all stem from a level of prefrontal cortex DA that has been raised higher than "normally transmitting." The average (non ADD) joe is not forcibly motivated or unnaturally productive; people treating ADD shouldn't expect to be, either.
 
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Not bad EM. But I got you beat.

It makes you feel all good and shit then you stop and you feel all shity. nah' mean?
 
The difference is that opioids release the DA indirectly through a strange mechanism, rather than directly as with amphetamines. Then, the dopamine that is released by opioids is eventually broken down in to norepinephrine, which is partly responsible for the typical opiate-induced insomnia.

This sounds fascinating - I had no idea about it. Do you happen to have a link to somewhere which elaborates about the mechanism? After a single session of opioid use, it doesn't feel like your dopamine is depleted like it does after amphetamine use. Is this partly why?

Also, what's up with the dopamine getting broken down into norepinephrine? I know that sometimes happens and sometimes doesn't but have no idea when, or why.

Would massively appreciate further explanation about this. I did put these questions into Google. The first result was this thread!
 
^ sorry I know it's appalling forum etiquette to bump one's own question but I've been wondering about this "strange mechanism" for the release of PFC dopamine by opioids pretty much every day for the last week. If anyone has an explanation, or a link to an explanation, I would massively appreciate it.
 
I dunno but it sure has great anti depressant properties. Another then that it seems to increase anxiety a bit. I can't smoke weed without getting panic attacks now
 
Opioids increase levels of prefrontal cortex Dopamine, relieving ADD much in the same manner as amphetamines do.

The difference is that opioids release the DA indirectly through a strange mechanism, rather than directly as with amphetamines. Then, the dopamine that is released by opioids is eventually broken down in to norepinephrine, which is partly responsible for the typical opiate-induced insomnia. Natural and semi-synthetic opiates don't have any appreciable affinity for 5-HT receptors.

People find opioids to be as good of an ADD medication as amps, and don't realize that combining a normally used ADD dosage of amphetamines with their opioids causes their low pf cortex DA levels to increase twofold, pushing it higher than the intended normal transmitting levels (normally focused), in to abusive, euphoric pf DA levels, causing focus and short term memory to once again deteriorate. If you are taking opioids, you will need a much lower dosage of amphetamines than non-opioid users would need to treat ADD. Combining the two increases the risk of amphetamine neurotoxicity through dopamine autoxidation, as dopamine is dopamine to the brain; it doesn't matter if it is increased by opioids or amphetamines.

Keep in mind that the purposes of ADD medications are simply to increase focus and alertness. The side effects of forced motivation, euphoria, anorexia, insomnia, anxiety, restlessness, neurotoxicity, and hyperfocus all stem from a level of prefrontal cortex DA that has been raised higher than "normally transmitting." The average (non ADD) joe is not forcibly motivated or unnaturally productive; people treating ADD shouldn't expect to be, either.
Wow, this is impressive! I have taken many different kinds of opiates/opioids;I'm currently on 100mcg Fentanyl patch and oxycodone immediate release (120-150mg per day). I've been taking the above meds for approximately 1.5 yrs.
I also take methylphenidate immediate release (80-100mg per day), and have been taking that for about 7 years.
I have AD/HD. I've always found oxycodone a bit uplifting and stimulating, especially in comparison to other narcotic pain meds. I always wondered why, and now I know! Sort of, anyway ;) I'm not sure I am on the same level as most of you who have posted on this thread...in terms of your knowledge and understanding regarding these chemicals (?) and how they work and interact (dopamine, norepinepherine, etc...)
EM, how do you feel about the methylphenidate along with my other meds? I've never had any problems, but I'm curious about what you said about Adderall. I'm guessing it's a totally unrelated situation, since ritalin isn't an amphetamine?
Hope you all have a wonderful day!
 
Opioids increase levels of prefrontal cortex Dopamine, relieving ADD much in the same manner as amphetamines do.

The difference is that opioids release the DA indirectly through a strange mechanism, rather than directly as with amphetamines. Then, the dopamine that is released by opioids is eventually broken down in to norepinephrine, which is partly responsible for the typical opiate-induced insomnia. Natural and semi-synthetic opiates don't have any appreciable affinity for 5-HT receptors.

People find opioids to be as good of an ADD medication as amps, and don't realize that combining a normally used ADD dosage of amphetamines with their opioids causes their low pf cortex DA levels to increase twofold, pushing it higher than the intended normal transmitting levels (normally focused), in to abusive, euphoric pf DA levels, causing focus and short term memory to once again deteriorate. If you are taking opioids, you will need a much lower dosage of amphetamines than non-opioid users would need to treat ADD. Combining the two increases the risk of amphetamine neurotoxicity through dopamine autoxidation, as dopamine is dopamine to the brain; it doesn't matter if it is increased by opioids or amphetamines.

Keep in mind that the purposes of ADD medications are simply to increase focus and alertness. The side effects of forced motivation, euphoria, anorexia, insomnia, anxiety, restlessness, neurotoxicity, and hyperfocus all stem from a level of prefrontal cortex DA that has been raised higher than "normally transmitting." The average (non ADD) joe is not forcibly motivated or unnaturally productive; people treating ADD shouldn't expect to be, either.

awesome read thanks for the info!
 
http://learn.genetics.utah.edu/content/addiction/mouse/

Grab the mouse on heroin and drop him in the test device.

It's cute, though for all I know they might get it a tiny bit wrong in their attempt to simplify (dopamine creating a sense of relaxation? I'd assume that's a separate affect of the opiate, but I am no expert.) Definitely one of my favorite sites.

I asked them which inhibitory neurotransmitter they had in mind, but they haven't yet replied. I'm going with GABA for now, but that's just a guess.
 
http://learn.genetics.utah.edu/content/addiction/mouse/

Grab the mouse on heroin and drop him in the test device.

It's cute, though for all I know they might get it a tiny bit wrong in their attempt to simplify (dopamine creating a sense of relaxation? I'd assume that's a separate affect of the opiate, but I am no expert.) Definitely one of my favorite sites.

I asked them which inhibitory neurotransmitter they had in mind, but they haven't yet replied. I'm going with GABA for now, but that's just a guess.

actually a cool link man, i'd suggest people to check it out, it's a little " young or simple " , yet very easy to understand and teaches you, really the basics behind the mechanisms of various drugs, cool.
 
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