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The Big and Bangin' Pseudo-Advanced Drug Chemistry, Pharmacology and More Thread, V.2

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DXM Afterglow...Is this possibly why it happens?

Some people say they feel nice rather than hung over after a DXM trip. Well, it's known that NMDA antagonism upregulates dopamine receptors. So could the increase in dopamine receptors possibly be why many people feel nice after the trip? Most people who claim to get hangovers are either regular users or took a massive dose.
 
I had a terrible hangover from DXM.. :(
It was my first time and I liked the actual high, but the day after was horrible.. Including headaches, chill's and anxiety.
The dose was around 300mg if I remember right.. Havent tried it again..... YET ;)
 
Moe-D said:
I had a terrible hangover from DXM.. :(
It was my first time and I liked the actual high, but the day after was horrible.. Including headaches, chill's and anxiety.
The dose was around 300mg if I remember right.. Havent tried it again..... YET ;)
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I'm the opposite. I took 350-400mg my first time and the high was terrible, lots of nausea in the beginning and there was zero euphoria, the dissociation was just uncomfortable(although synthetic weed's dissociation was euphoric to me), and I just felt retarded.

The afterglow was nice and relaxing, conversely.
 
Amphetamine without Cortisol Release, How Would It Be Different?

I was wondering if there was an amphetamine that didn't release cortisol how would its effects be different from standard amphetamine that releases cortisol?

The things I can think of are that it probably wouldn't lead to as much weight loss, maybe less immune system problems (This is from recreational dosing!) and maybe less memory enhancement as I know cortisol plays a part in memory function ( http://www.ncbi.nlm.nih.gov/books/NBK3907/ ).

I can't really think of much else at the moment.
 
I always thought that the cortisol release of amphetamine is caused by downstream activation of dopamine receptors - i.e. amphetamine itself doesn't release cortisol, dopaminergics in general do
 
Anoymator said:
Anybody know why pregabalin at high doses yields some heavy closed eye visuals? This effect has been reported a few times and it tends to be of a movie-like nature in that you can see how themes develop.
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Awww yes. Here comes the lyrical train again.

Mafaka, I am seeing a freaking movie when I close my eyes. Black and white, oldschool Charles Chaplin style. I even get subliminal messages in the movie, random words.

For the love of Snoopy, any one know the MOA for the CEVs? I tried asking Charles Chaplin; he said it's NMDA antagonism but then I told him that pregabalin is not known to modulate the NMDA receptor so he shrugged his shoulders, winked at me and evaporated.

Edit: Serious question, with open eyes I feel stoned but it is when I close my eyes that the show begins in seconds.

2nd edit: he also told me it's Charlie, not Charles. You've got to be kidding me.
 
Anoymator said:
Awww yes. Here comes the lyrical train again.

Mafaka, I am seeing a freaking movie when I close my eyes. Black and white, oldschool Charles Chaplin style. I even get subliminal messages in the movie, random words.

For the love of Snoopy, any one know the MOA for the CEVs? I tried asking Charles Chaplin; he said it's NMDA antagonism but then I told him that pregabalin is not known to modulate the NMDA receptor so he shrugged his shoulders, winked at me and evaporated.

Edit: Serious question, with open eyes I feel stoned but it is when I close my eyes that the show begins in seconds.

2nd edit: he also told me it's Charlie, not Charles. You've got to be kidding me.
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Well it really changes sleep architecture, particularly enhancing slow wave sleep, so I would hazard a guess it's a "pipe dream" like phenomenon. Perhaps it knocks your neuronal activity down into REM mode?
 
Epsilon Alpha said:
Well it really changes sleep architecture, particularly enhancing slow wave sleep, so I would hazard a guess it's a "pipe dream" like phenomenon. Perhaps it knocks your neuronal activity down into REM mode?
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Thanks for replying guys. Sorry for the post last night, was utterly fucked on 500mgs of pregabalin. I'm using it to wean down from a high tramadol use and it is helping. It knocked my ass out even after 6 hours of having ingested it, even though without the pregabalin I'd be withdrawing hardcore from the tramadol. Love this drug, only thing is that it has caused me to have clots so I always inject a fast anticoagulant if im going to use high doses.

The CEVS are very real and sometimes even too violent as they are moving too fast. I was chilling out with Charlie Chaplin and it felt like I was drifting into sleep, then I opened my eyes and everything faded and I just felt stoned. I really do think there is something going with REM sleep because while I am conscious, I can only hold the CEVs for 40 mins before passing out.

I like the glutamate theory, how would that cause CEVs? How about what Chaplin told me (LOL)? Would you advanced folks think pregabalin could cause some activation in the NDMA receptor at all? I would not be the first one to report that high doses of pregabalin feel like ketamine.

I really hope that a trend of abusing pregabalin to get CEVs is not started as the drug is fairly easy to get and it will be going generic in 2013, but the drug is worth the occasional use to get some wicked CEVs and feel stoned for 8 hours.
 
thenightwatch said:
if you didn't realize, the NMDA receptor is a glutamate receptor.
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I am not advanced (just curious in terms of drug pharmacology) and while I am aware that they are both interrelated, I don't know how the glutamate theory would explain the CEVs caused by pregabalin as for all I know this drug is not known to interact with this receptor (but then, I could easily be wrong). If you know the modus operandi, by all means, enlighten me.

Pregabalin seems to be a drug which is still not fully known as to how it works which makes me even more curious to know any suspected actions which could yield this notable side effect (I always get CEVs at high doses and so do others, but the drug is very expensive hence the online user experience reports are not plenty).
 
i'm not really too advanced either. this is from the wikipedia entry on pregabalin, tho:

Pregabalin decreases the release of neurotransmitters including glutamate, noradrenaline, substance P and calcitonin gene-related peptide.
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not QUITE the same as NMDA antagonism. but close? like i said, i'm not too advanced either. :)
 
What neurotoxic properties of NMDA antagonists / DRIs are you talking about? To my knowledge, they're not. (no Olney's Lesions in primates, ketamine as an antidepressant that promotes neuron growth, many trials of NMDA antagonists for stroke neuroprotection, NDRI drugs being comparatively very safe to releasing agents, etc)

Many 5-HT agonistic compounds are cerebral vasoconstrictors, but it's not always bad wrt neurotoxicity. It would however increase b.p. and hence stroke risk if used regularly.
 
I was under the impression that the documented impairment of memory and cognitive function in regular users of ketamine implies neurotoxicity, even of the specific mechanism is not understood. Also there have been a couple studies that have suggested mechanisms whereby ketamine can cause adverse effects on the CNS. I've linked to two of them below.

http://www.ncbi.nlm.nih.gov/pubmed/17418473

http://www.ncbi.nlm.nih.gov/pubmed/7976530
 
What do you all think could be the reason why a good % of people report an instant mood lift with tramadol? Tramadol (as opposed to O-desmethyltramadol) is a very weak opioid so this mood lift can't be fully attributed (if at all) to opiate receptor activity. I have read many reporting this effect about 20-30 minutes after ingestion of doses between 150- 300mgs and in one single dose (not spaced out to maximise the opiate effect).
 
Anoymator said:
What do you all think could be the reason why a good % of people report an instant mood lift with tramadol? Tramadol (as opposed to O-desmethyltramadol) is a very weak opioid so this mood lift can't be fully attributed (if at all) to opiate receptor activity. I have read many reporting this effect about 20-30 minutes after ingestion of doses between 150- 300mgs and in one single dose (not spaced out to maximise the opiate effect).
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Probably because Tramadol is also an SNRI.
 
vortex30 said:
Probably because Tramadol is also an SNRI.
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Yes but, as far as I am concerned, SNRIs take weeks to yield the mood lift, not 20 minutes, plus the mood lift from tramadol is irrespective of having taken it other times. Likewise, the reported mood effect of SNRIs seems to be more towards a stabilized "no-highs & no-lows" effect which is not same as that of tramadol.
 
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