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Amphetamine Neurotoxicity and Tolerance Reduction/Prevention II

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Aetherius Rimor said:
Ok this seems to be almost a recurring theme in stuff I read about, as far as addiction goes, so I'm wondering if you have any further knowledge on this subject or have articles I could learn more from.
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If I find a solid paper on it I'll post it, but try google'ing around the topic. There's a lot of good evidence, just no good review article >:(

Everyone that I know who has been diagnosed bi-polar, seems to have one of two extremes with drug addiction. Either they're like me, and the couple bi-polar people I actually will associate with, and have it seems no reward response from taking drugs that normally induce rewards. Or they have the exact opposite and have extreme addiction issues, where they -have to have it- and get easily addicted.
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I hear you man, its kind of like schizophrenics and autistic kids (google "I told you I was hardcore" for a suspected case)

I know I've brought this up at bluelight before in other threads, but I still haven't gotten a satisfactory conclusion to this curiosity. It's a great trait to have, but with how confusing it is, I have an insane desire to know -why-.

Edit: Side note, is there a link you can share that goes more in depth of the differences between sensitization and tolerance, or would you be willing to describe them a little more? I'm not sure I follow, but as I currently interpret what you're saying, sensitization is an increased desire for it, and tolerance is a reduced effectiveness of it? If that's the correct meanings, it would explain my experience with opiate/benzo to say that I gain no sensitization, but do gain tolerance, correct?
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Same here, and I wish I had a good link for it. Sensitization is weird in humans in the fact that its a completely separate process from tolerance, and mainly manifests as behavioural changes as far as I know. There's a link near the start of the thread I posted regarding amphetamine sensitization in humans after 3 uses if you want some reading.
 
This is a really interesting thread. I recently found a study at my uni that correlates the # of DA receptors and impulsivity to increased addictive behavior in rats. It was a short summary but the interesting part is this ":
impulsive rats, which had never before been exposed to cocaine, self-administered more of the drug than non-impulsive rats. Moreover, the higher the rats’ pre-drug impulsivity levels, the fewer dopamine D2/3 receptors they had in the nucleus accumbens, a brain structure known to have a role in motivation and reward.
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That's pretty cool shit to me. It provides more basis for the belief that impulsive people, particularly the ADD population, are theoretically more inclined to have an addictive personality. The first line of treatment is usually stimulants and since most stims I know are dopaminergic, It could be safe to assume that is the reason most medicated ADD'ers are less likely to self-medicate with other drugs. And the fact that depression is a comorbidity very commonly observed with people with ADD, its plausible to hypothesize the 2 are related to having low dopamine levels/receptors

I hope that made sense lol
 
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n-acetyl-cystiine (NAC). Has using this with amps been discussed?

IIRC, it's used as a first line "antidote" for APAP poisoning in hospitals.
A friend said it seemed to tune down a certain number of negative effects and crash associated with methamp and amp, but not at all with 2-FMA.

I'm still reading about it, so I know very little atm.

Edit - He also said that it removes hangovers from alcohol and/or prevents them.
 
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crestfallen said:
This is a really interesting thread. I recently found a study at my uni that correlates the # of DA receptors and impulsivity to increased addictive behavior in rats. It was a short summary but the interesting part is this ":

That's pretty cool shit to me. It provides more basis for the belief that impulsive people, particularly the ADD population, are theoretically more inclined to have an addictive personality. The first line of treatment is usually stimulants and since most stims I know are dopaminergic, It could be safe to assume that is the reason most medicated ADD'ers are less likely to self-medicate with other drugs. And the fact that depression is a comorbidity very commonly observed with people with ADD, its plausible to hypothesize the 2 are related to having low dopamine levels/receptors

I hope that made sense lol
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Lol no worries it made sense, its pretty interesting looking at the roles of D2 like receptors (D2, D3, and D4) in impulsiveness and social roles. Here's some interesting info on it that pretty much damns the whole "amphetamine for social anxiety" movement as well (sorry MeD, D2 downregulation is a bitch :/).

http://www.nature.com/neuro/journal/v5/n2/abs/nn798.html
 
Aetherius Rimor said:
Edit: Side note, is there a link you can share that goes more in depth of the differences between sensitization and tolerance, or would you be willing to describe them a little more? I'm not sure I follow, but as I currently interpret what you're saying, sensitization is an increased desire for it, and tolerance is a reduced effectiveness of it? If that's the correct meanings, it would explain my experience with opiate/benzo to say that I gain no sensitization, but do gain tolerance, correct?
Click to expand...

http://www.ncbi.nlm.nih.gov/pubmed/18486243 Review of rat amphetamine model of schizophrenia
http://www.sciencemag.org/content/207/4428/329.short
Most of it seems to stem from inadvertent activation of the stress response rather than activation of the reward pathways
Functional Magnetic Resonance Imaging Investigation of the Amphetamine Sensitization Model of Schizophrenia in Healthy Male Volunteers
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Amphetamine kind of seems to mimic intense longterm stress in abuse settings which seems to be similar to intense negative experiences seen commonly in the onset of bipolar/schizophrenia. Interestingly enough, it appears to be a more corticosteroid/5HT/NE/Glu mediated process to me than the traditional dopamine theories.
 
Epsilon Alpha said:
http://www.ncbi.nlm.nih.gov/pubmed/18486243 Review of rat amphetamine model of schizophrenia
http://www.sciencemag.org/content/207/4428/329.short
Most of it seems to stem from inadvertent activation of the stress response rather than activation of the reward pathways


Amphetamine kind of seems to mimic intense longterm stress in abuse settings which seems to be similar to intense negative experiences seen commonly in the onset of bipolar/schizophrenia. Interestingly enough, it appears to be a more corticosteroid/5HT/NE/Glu mediated process to me than the traditional dopamine theories.
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Excuse my ignorance, but what does "Glu" stand for.. Glucosamine?
 
I am quite under-educated compared to most of you, but recently I have noticed that drinking a moderate amount of alcohol before, during and after a meth session can decrease the duration and effects of the amphetamine.

Could this be due to the fact alcohol increases the speed of dopamine transmission thus speeding up effects of meth or is it more the anti-GABA effects?

EDIT: I do not read every bumped thread every day so soz if I have missed the answer to my question and you assume Im retarded. UTFSEncylopedia I know :(
 
I'm assuming it's going to be a combination of both GABA/NMDA effects that Alcohol has.

Being a sedative due to GABA, and the neuroprotective qualities of NMDA. Speculation on my part based on what I've read so far, but that's my initial guess.
 
Dizmal said:
I am quite under-educated compared to most of you, but recently I have noticed that drinking a moderate amount of alcohol before, during and after a meth session can decrease the duration and effects of the amphetamine.
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Alcohol lowers the pH of your urine and is a diuretic. These effects increase the renal excretion of amphetamines and shorten the duration of action. Taking a lot of vitamin C to acidify your urine would have the same effect. (in fact for this reason, amphetamine overdose victims are given vitamin C or ammonium chloride through an IV drip in the hospital)
 
Dizmal said:
I am quite under-educated compared to most of you, but recently I have noticed that drinking a moderate amount of alcohol before, during and after a meth session can decrease the duration and effects of the amphetamine.

Could this be due to the fact alcohol increases the speed of dopamine transmission thus speeding up effects of meth or is it more the anti-GABA effects?

EDIT: I do not read every bumped thread every day so soz if I have missed the answer to my question and you assume Im retarded. UTFSEncylopedia I know :(
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DexterMeth said:
n-acetyl-cystiine (NAC). Has using this with amps been discussed?

IIRC, it's used as a first line "antidote" for APAP poisoning in hospitals.
A friend said it seemed to tune down a certain number of negative effects and crash associated with methamp and amp, but not at all with 2-FMA.

I'm still reading about it, so I know very little atm.

Edit - He also said that it removes hangovers from alcohol and/or prevents them.
Click to expand...

anyone?
 
polymath said:
Alcohol lowers the pH of your urine and is a diuretic. These effects increase the renal excretion of amphetamines and shorten the duration of action. Taking a lot of vitamin C to acidify your urine would have the same effect. (in fact for this reason, amphetamine overdose victims are given vitamin C or ammonium chloride through an IV drip in the hospital)
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Thanks! Wasn't aware of that. I'm sure the things I mention have some effect (even if negligible) on dampening the experience, but that definitely explains the shorter duration.
 
Not sure an "antidote" should ever be used long term, no?
Sounds like something good to on hand.

I was not thinking long term or high doses at all though. If it works so well, I can see how it would quickly get out of hand and cause harm.
 
NAC prevents hangovers because it binds to acetaldehyde, the toxic metabolite of alcohol.

http://www.ncbi.nlm.nih.gov/pubmed/8833231
All known pathways of ethanol metabolism result in the production of acetaldehyde, a highly reactive compound. N-acetyl cysteine, an analogue of the dietary amino acid cysteine, binds acetaldehyde, thus preventing its damaging effect on physiological proteins.
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Epsilon Alpha said:
We talked a little about NAC, and my take on it was its promising short term but has some potential to be negative long term at high doses.
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Here's an abstraction for you, Epsilon: What if you had to advocate the most effective NAC supplement protocol -- what would that entail?

Without going into explicit details, I take NAC for a WIDE variety of reasons, and have nestled it in as a top 10 health supplement of mine over the last 1.5 years. I want to (or maybe I don't) continue taking it at ~1200 mg a day. :\
 
Tussmann said:
Here's an abstraction for you, Epsilon: What if you had to advocate the most effective NAC supplement protocol -- what would that entail?

Without going into explicit details, I take NAC for a WIDE variety of reasons, and have nestled it in as a top 10 health supplement of mine over the last 1.5 years. I want to (or maybe I don't) continue taking it at ~1200 mg a day. :\
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To be honest man, I hardly have any time to research any more but I haven't seen any data either way. If you've figured out something that works for you for several reasons, by all means keep on it. I just wouldn't advocate long term use of it for amphetamine toxicity only, and I'd also maybe advocate for taking it before your amp just to make sure it gets absorbed prior.
 
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