Given that dopamine is no longer regarded by many neuroscientists to be a pleasure neurotransmitter after all.
Please, I need more info about this assertion,where can I find more scientific articles about this subject?
N&PD Moderators: Skorpio | thegreenhand
Given that dopamine is no longer regarded by many neuroscientists to be a pleasure neurotransmitter after all.
im not familiar with opiates but it seems heroin users dont do much when high and just have their life passing by
You have obviously never seen someone who is withdrawing from heavy amphetamine use.
All of my whats.
Seems weird to me. Even though I wasn't particularly addicted to amphetamines. I still used them for about a year and a half, 2-3 times a week, and I didn't notice any kind of physical withdrawals other than fatigue for a short amount of time. Moderate depression and boredom hell were about the only pronounced ones. Hell even the cravings were fairly easy to deal with.
I was always under the impression that Amphetamine withdrawals were mental more so than physical.
I don't see how activation of opiate receptors play such a huge role in the addictive nature of amphetamines. If you consume a large dose of amphetamines - would opiate receptors also be activated at higher levels? Would this not counteract the side effects of amphs such as dilated pupils, tachcardya and anxiety?
Or are opiate receptors not helpful for the control of this in the body? Correct me if I'm wrong.
Both amphetamine and opiates though can make some pretty big changes to the immune system to an addict.If AMP gives pleasure through opiate release then why doesn't AMP give an opiate-like withdrawal upon cessation?
Are there any studies investigating if and to what degree amphetamine euphoria is mediated through said opioid release i.e. can the euphoria be blocked with opioid antagonists? As you probably know alcohol euphoria can be completely blocked with naltrexone, right? If also AMP euphoria can be blocked it raises the question: Can all drug induced wellbeing be blocked with naltrexone and thus be mediated trough opioid release?
Thank you so much for this study, I have searched for it quite a few times before, this reassures me on my hypothesis that mu receptor activity does play some role in subjective effects, it just all connects. Very appreciative endotropic!Ethanol, nicotine, amphetamines, cannabinoids, opiates (no really), but probably not serotonergics.
Reference for amphetamine:
Effects of naltrexone on the subjective response to amphetamine in healthy volunteers.
http://www.ncbi.nlm.nih.gov/pubmed/15538132
And nicotine:
Naltrexone alteration of the nicotine-induced EEG and mood activation response in tobacco-deprived cigarette smokers.
http://www.ncbi.nlm.nih.gov/pubmed/17696684
I don't know if human studies have been done with serotonergics + naltrexone, but you can find the animal data.