I don't think you need to go and say that I don't know what I'm talking about. We haven't even formally met nor do you know anything about my background, educational level or anything else. So please don't flame.
Thanks by the way for posting the links. However, I still don't see anything in your links that says SSRI
+MDMA = seratonin syndrome.
Here is a post from Drug
Dustbin off of bluelight that is very helpful and very much coincides with what my doctor was saying.
>SSRI's work by stopping the seratonin reuptake in the brain.
SSRIs will prolong the effects of transmitter in synaptic cleft by interfering with
the transporter protein. They doesn't completely block reuptake.
>The idea is for those that are depressed is that by reducing the amount of seratonin
>reabsorbed back into one's neurochemical system (and thereby increasing the amount of
>seratonin present), an increased amount of seratonin will help people feel better
>(With the help of therapy, of course. Very rarely will SSRI's work without the will
>and help of both the user and his/her doctor.)
require on average couple of weeks to exert an effect, so the
increased synaptic serotonin
can't explain solely their antidepressive effects.
It has been suggested that the antidepressive effects are due to decreased responsiveness
of somatodendritic 5-HT1A autoreceptors and decreased function of terminal 5-HT
autoreceptors. So, whatever it is, it's most likely due to adaptive changes.
>Okay, now for the role of Ecstasy
. Ecstasy works by flooding the synapse in the brain
>with seratonin. (again, as we all know.) Because Ecstasy uses the actual reuptake
>transporter mechanism to cause seratonin release, obviously any sort of chemical
>(Like an SSRI) blocking that mechanism (Which SSRI's do,) with a higher affinity
>for it (Like Ecstasy) will severely reduce or completely eliminate the affects of the
You must remember that the biochemical interactions between the receptor and the
substrate(s) are concentration-dependent (in the case of competitive substrates).
In _In vitro_ test MDMA
can displace paroxetine
from its binding sites.
>Ecstasy (beyond the threshold dose of ~40-60mg) without the presence of SSRI's
>generally drains a large amount of the brain's seratonin for 12-24 hours, and the brain
>has generally not reached full seratonin levels for up to a week afterwards.
Please, give me some journal references about this serotonin draining in humans.
There is one new study about chronic MDMA use on striatal serotonin levels, but
I haven't been able to read that study yet, and I assume you neither have read it.
I'll include the abstarct here:
"The authors found that striatal levels of serotonin and those of its metabolite
5-hydroxyindoleacetic acid were severely depleted by 50 to 80% in brain of a chronic
user of methylenedioxymethamphetamine
(MDMA) whereas concentrations of dopamine
within the normal control range. Our data suggest that MDMA exposure in the human can
cause decreased tissue stores of serotonin and therefore some of the behavioral effects
of this drug of abuse could be caused by massive release and depletion of brain serotonin".
>SSRI's "downregulate" (inhibit the efficiency & the ability) of seratonin reuptake
>transporters. This means SSRI's affect your brain's seratonin system in a negative
>way as well as a positive way; the idea is that the positive effects outweigh the
>negative i.e. higher seratonin levels outweight the fact that your brain isn't using
>it as efficiently. Basically this means that even for MONTHS after one quits taking an
>SSRI, the brain is less efficient at using seratonin. Those who go off SSRI's and take
>E, even MONTHS later, will most likely have a REDUCED roll, regardless of the amount of
>E you take.
There is some evidence that serotonin transporter (SERT) binding is decreased
in some brain regions in animals treated continuously with SSRIs. I would like to see
some references about the long-term effects of SSRIs on SERT function. Do you have
them? It is interesting to notice, that according to one recent study, the SERT
and DAT binding is significantly increased in acutely absistent cocaine
patients, suggesting compensatory up-regulation of SERT and DAT (dopamine transporter).
You said, "the fact that your brain isn't using it [serotonin] as efficiently".
Can you clarify this comment?
And get the latest issue of Neuropsychobiology, it's dedicated to MDMA. It contains
lots of interesting topics.