Comment · Thu, October 10, 2013
So my mum tried my MXE
Original post in this thread
throwaymexxy · 124 points
My mum has depression, and I told her MXE was a fairly potent antidepressant to my knowledge. Yesterday she asked me for a dose and now she's next to me, she was surprised by how potent it was.
She's having a good time, I've made her aware it's not going to be a quick fix for anything but for now she's enjoying the relief. I did make sure I had explicit consent from her. I'm not too sure why I let her do it but I am curious about whether the 'afterglow' will help her.
I'll update this post with any results. She has used some drugs in the past, to my knowledge: MDMA, Amphetamine paste, weed and some unknown hallucinogen.
Update: Now she is coming down she feels that it wasn't on the level she'd hoped but it was by no means a bad experience at all. I just think she had different expectations of what it would be like and wasn't aware of what the high would be like. She seems quite content and happy right now though.
Update 2: She says she still feels happy and slightly under the influence and that it was pleasurable. She says she feels a bit more relaxed and mellow than before she took it.
What they were answering
Borax · 2 points
That's 5HT-2 and each is much more selective for NMDA, meaning the serotonergic effects are likely to be negligible.
PCP has selectivity of 0.02 for NMDA over SERT though, ketamine has no affinity. MXE on the other hand has 0.54 selectivity which is quite significant.
u/MisterYouAreSoDumb
The first study I linked showed ketamine blocks the activity of the SERT.
These data support the contention that the primary direct effect of ketamine on serotonergic systems is the blockade of 5-HT uptake and that blockade of 5-HT uptake may mediate some of the behavioral effects of ketamine, such as analgesia.
Here is another study showing the same thing.
The present study demonstrates that subanesthetic ketamine selectively enhanced serotonergic transmission by inhibition of SERT activity.
Our results demonstrate that both ketamine and propofol inhibited SERT and NET function
Inhibition analysis showed that ketamine significantly inhibited the uptake of all three monoamine transporters in a dose-dependent manner. The Ki (inhibition constant) values of ketamine on the norepinephrine, dopamine, and serotonin transporters were 66.8 microM, 62.9 microM, and 162 microM, respectively.
Then there is PCP, where the metabolites are most likely to blame for the SERT inhibition.
http://www.ncbi.nlm.nih.gov/pubmed/8736633/
PCP and its metabolites inhibited the uptake of 5-HT and the binding of paroxetine in rat brain, while they failed to inhibit either 5-HT binding to 5-HT1 receptors or ketanserin binding to 5-HT2 receptors. The trans-isomer of 4-phenyl-4-(I-piperidinyl)cyclo-hexanol (trans-4-PPC), the major metabolite of PCP, rather than PCP itself, inhibited 5-HT uptake most potently.
Amphetamine and PCP both dose dependently increased dialysate levels of dopamine (DA) and 5-HT in the nucleus accumbens, striatum and frontal cortex (FCX) of freely moving rats, but PCP was proportionally more effective than amphetamine in elevating levels of 5-HT vs. DA in the accumbens.
In any event, my point was that most people don't know that both ketamine and PCP inhibit the SERT, and not only lead to increases in 5-HT, but DA as well. Many people just think of them as NMDA receptor antagonists.