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Moclobemide for easing the MDMA blues.

Kball, I too highly agree that your doctor is foolish to state that it should be fine in combination. So I would be very careful, you've got it away with it so far, but all it might take is one stronger pill to send you over the edge into serotonin syndrome.
 
Tianeptine also looks promising in combating a MDMA comdown. Maybe with an even better level of safety and less side effects? Any one care to comment?
 
Tianeptine bugs the heck out of me.

It's so odd, I don't even know how to consider it in this respect. I'm worried that if SSRIs block MDMA's effects, Tianeptine might cause death.

No idea why though, it doesn't make sense, not logical.
 
^ I don't like the idea at all with combining it with MDMA. I find the explanation interesting on wiki,

"newer research suggests that its direct action is actually alteration of AMPA glutamate receptor activity, which then leads to enhanced serotonin reuptake via a downstream mechanism which has yet to be fully characterised, but seems to involve altered neuroplasticity and release of BDNF."
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From this perspective it may be safe. Though serotonin reuptake may not be the right way to tackle the after effects of MDMA. But I do like the sound that it releases brain-derived neurotrophic factor, which could help with any post MDMA neurotoxicity.
 
There was a good study that looked at SAR of SSREs, and it was a fairly limited range of compounds that had the property at all. I forget the details. I think mad_scientist was the one who mentioned this, but my memory is terrible.

No, it's not the right way at all- it's probably completely useless, actually.

The reason I think that tianeptine might even be a little dangerous is because with the released 5HT being taken back up more and faster, less of it should be getting metabolised, which may mean your body has more of it to work with, and maybe it makes some of the worse aspects of MDMA- the body temp increase is the main one- even worse because of the extra 5HT to work with.
 
Well mihjt be a bit offtopic but for me a small supplement of desoxypipradrol (max 1mg) and 2x 150mg or so of neurontin or lyrica really makes life easier after a decent roll. Don't suffer from much depletion-effects myself though, but this was one to remember. maybe on day 3-4 half your reimen on both substances... And eat bananas! :)
 
me too :) Gotta hit the deck soon, almost 8,30 in the morning, did lotsa homework... so tomorrow it is lyrica ans desoxybreakfast i guess...
 
Next you'll tell me that I shouldn't have a shot of vodka to get rid of my hangover.
 
permastoned said:
^ What an awesome psych haha.. Can you tell me who he is :p

Ok basically, the main two effects of d-amp are release of noradrenaline and dopamine. Dopamine is responsible for the pleasurable feelings of the stim, whereas noradrenaline tends to be responsible for the irritability (especially later on), the insomnia, that weird yawny feeling, shrinking of your dick, loss of appetite etc. You will know the feeling if you take an NRI such as atomextine or reboxetine. They suck balls.

What dose of moclobemide are you on?

There are two forms of MAO - A and B.

Moclobemide mostly inhibits MAO A. MAO A is responsible for dopamine, serotonin, and norepinephrine. So when you use it to potentiate a stim, you are potentiating both the good effects, but also (in my opinion, the bad effects).

Of those 3 neurotransmitters, MAO B only metabolises dopamine. As such, with selegiline (a selective inhibitor of MAO B), you will only potentiate the good effects. However, the effect on serotonin from moclobemide would be missing, so it is a bit of a toss up.
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true, but selegiline inhibits dopamine breakdown much better than moclobemide. I think its almost 98% inhibition at 10mg.

I have always wondered. Does MAO-A inhibit dopamine just as well as MAO-B?

Myabe if someone wanted the effectiveness of something like Parnate or Nardil but was worried bout the sides could take low-dose selegiline with an SSRI and have a similar effect to the "gold standard" MAOIs
 
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PetersKeys said:
true, but selegiline inhibits dopamine much better than moclobemide. I think its almost 98% inhibition at 10mg.

I have always wondered. Does MAO-A inhibit dopamine just as well as MAO-B?

Myabe if someone wanted the effectiveness of something like Parnate or Nardil but was worried bout the sides could take low-dose selegiline with an SSRI and have a similar effect to the "gold standard" MAOIs
Click to expand...

Firstly, by saying 'inhibit dopamine' you are being misleading. What you mean to say is 'inhibit dopamine metabolism'.

Secondly, the 98% inhibition value that you quote refers to the inhibition of MAO-B enzyme, not the total inhibition of dopamine metabolism. Inhibition of dopamine metabolism to that degree would likely cause death. Dopamine is not only metabolised by MAO A and MAO B, it is also metabolised by COMT and dopamine beta-hydroxylase. MAO A and MAO B are definitely equal in terms of their dopamine and tyramine metabolism - I just checked one of my pharmacology texts - Goodman & Gilman's pharmacological basis of therapeutics.

Whilst 10mg of selegiline will inhibit 98% of MAO B (according to you), this is not the reason it is more effective at metabolising dopamine than moclobemide. In fact you will find that "a single 300 mg dose of moclobemide inhibits 80% of monoamine oxidase A (MAO-A) and 30% of monoamine oxidase B (MAO-B)". Do the maths. Given that MAO A and MAO B metabolise dopamine equally, this equates to less dopamine metabolism.

Where moclobemide falls down is in its reversibility. Why? Because the concentration of moclobemide must compete with the concentration of dopamine to bind to MAO A and MAO B. As such, the larger the increase in dopamine concentration, the more likely each dopamine molecule is to get metabolised than moclobemide is to inhibit the enyme - the two substrates must compete for the same binding site! In this way, moclobemide is self limiting in essence, to a degree at least.
 
permastoned said:
Firstly, by saying 'inhibit dopamine' you are being misleading. What you mean to say is 'inhibit dopamine metabolism'.

Secondly, the 98% inhibition value that you quote refers to the inhibition of MAO-B enzyme, not the total inhibition of dopamine metabolism. Inhibition of dopamine metabolism to that degree would likely cause death. Dopamine is not only metabolized by MAO A and MAO B, it is also metabolized by COMT and dopamine beta-hydroxylase. MAO A and MAO B are definitely equal in terms of their dopamine and tyramine metabolism - I just checked one of my pharmacology texts - Goodman & Gilman's pharmacological basis of therapeutics.

Whilst 10mg of selegiline will inhibit 98% of MAO B (according to you), this is not the reason it is more effective at metabolizing dopamine than moclobemide. In fact you will find that "a single 300 mg dose of moclobemide inhibits 80% of monoamine oxidase A (MAO-A) and 30% of monoamine oxidase B (MAO-B)". Do the maths. Given that MAO A and MAO B metabolise dopamine equally, this equates to less dopamine metabolism.

Where moclobemide falls down is in its reversibility. Why? Because the concentration of moclobemide must compete with the concentration of dopamine to bind to MAO A and MAO B. As such, the larger the increase in dopamine concentration, the more likely each dopamine molecule is to get metabolized than moclobemide is to inhibit the enyme - the two substrates must compete for the same binding site! In this way, moclobemide is self limiting in essence, to a degree at least.
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I'm sorry, I had meant inhibit dopamine breakdown, forgot to type in that word. However I have read MAO-A is mostly in the gut while MAO-B is mostly in the brain, hence there is an issue with inhibition of MAO-A in the brain. I didn't know they inhibited breakdown equally. I had always thought MAO-A concentrated more on serotonin and NE, while mildly effecting dopamine, while MAO-B concentrated more on dopamine and PEA rather than seratonin and NE cause it says on wiki:

A single 300 mg dose of moclobemide inhibits 80% of monoamine oxidase A (MAO-A) and 30% of monoamine oxidase B (MAO-B),[3] blocking the decomposition of norepinephrine, serotonin and, to a lesser extent, dopamine




Would higher doses of moclobermide increase better competition for the moclibermide to bind? It reverses in 24 hours I think, while the irreversible inhibits for around 2 weeks I believe. Selegiline deavtices MAO-B for around 2 weeks, so It wouldn't really be competing with the dopamine I think.

It seems with moclobemide you would have to increase the dose a little bit everytime your dopamine levels increase. I hear allot of reviews saying that it works well for mild depression but isn't to great for severe depression.

http://www.revolutionhealth.com/drugs-treatments/rating/aurorix-moclobemide
 
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