Hi. I'm gonna post this to any newsgroup I can find that answers the
keyword search "nmda". Just recently I read a great article that suggests
using a 30mg/kg dose of supplemental magnesium to receive some of the
same effects as dizocilpine(mk-801). I think this has some astounding
implications, but if you read medical articles you know how they can
downplay that kind of stuff. So heres what I'm gonna do. Explain how Mg
is supposed to work. Ramble off some practical applications, and
hopefully get some slams/supportful posts/emails in response. Little
disclaimer here, some of these theres evidence for and some of these are
totally theoretical(blind guesses), that said here goes.
1. Good evidence that approx 2g magnesium reverses tolerance to ethanol.
My guess is that it also reverses tolerance to ketamine, ghb, and any
of the dopaminergics in general.
2. It also works as a calcium channel blocker. I'm not sure if this is a
necessary link, or merely a coincidence.
3. I'm guessing here but I also think it would work as a 5-ht1a agonist.
If you guys want to check medline I used "dizocilpine" "nmda" "tolerance"
"magnesium" "calcium" "dopamine" "serotonin" ect. Basically once your
convinced magnesium similarly blocks nmda channels start linking that
with others. The huge problem is mg does so many other things.
4. Alcoholics have upregulated nmdas(among other things) so mg might help
withdrawal(or make it worse if I'm backwards)
5. Theres ALOT of evidence that dizocilpine is supposed to work as an
antidepressant in the "chronic stress" model of depression(meaning
dopamine dependent". I'm not sure if this also applies to mg. It
definitly blocks nmdas, but it also blocks calcium channels making ca2+
dependent neurons(most of them) pretty impaired. But now my thinking is
that this is part of the process. Over a month dizocilpine upregulated d1
and d2 receptors, so maybe its the initial blocking that does this.
Basically I think mg acts as a calcium channel blocker, nmda blocker,
5ht1a agonist. I'm not sure if this is coincidence or necessary(like
noticing that almost all alpha-2blockers are 5-ht1a agonists and vice
versa). But it should do the following things. Stop depletions from
cocaine/amphetamine(by stopping release) but then its also supposed to be
an immediate inducer of sterotyped(dopamine) behavoir. I'm lost.
Coincidentally I also think that mg is about the biological opposite of
caffeine in many ways. Along with adenosine mg also stops DA release,
and caffeine blocks the adenosine speeding DA release(yes its recently
been proven that caffeine does alot of the same things as speed, No I
dont know why theres a legal difference.) My big intrest is in having a
new antidepressant in the arsenal, and also the ways it affects alcohol
-------------------==== Posted via Deja News ====-----------------------
http://www.dejanews.com/ Search, Read, Post to Usenet