Dbc
Mar 19, 2007, 05:52 PM
After much research and a recent paper published on ketamine and depression a friend of mine has decided to run a live experiment using a common 'legal' NMDA antagonist to treat alprazolam withdrawal/dependence. I warned him of the dangers involved but he has his mind set on trying this and as he said "dependence is a dirty and nasty thing to have to live with, if this works it may not help the world but maybe a small group of people".
Is this as crazy as it sounds? I've read papers on opiate/diazepam addiction and NMDA antagonists so i understand where he's coming from but it seems a little extreme to put the theoretical into practice.
lucid_dream
Mar 19, 2007, 06:11 PM
common 'legal' NMDA antagonist? As in dextromethorphan-containing cough syrup? Bear in mind that not all NMDA antagonists have the same effect, and that the drugs used in the studies you and your friend read about over opiate/diazepam addiction are not OTC.
DXM is definitely not the optimal NMDA antagonist to experiment around with. Also, see
http://www.jabfm.org/cgi/content/full/19/3/320
Orbz
Mar 19, 2007, 08:28 PM
In regards to NMDA anatagonists (ketamine), do you think there is a link between the memory deficits induced by nmda anatgonism with the anti-depressant effects and the side effects of ECT, including memory loss, contributing to the efficacy of ECT?
lucid_dream
Mar 19, 2007, 09:10 PM
I don't know enough about how ECT effects brain function to say. NMDA antagonists usually activate limbic-related areas, and my guess would be that memory dysfunction is due to hippocampal dysfunction (perhaps through overactivation or activation of inhibitory circuitry). I'm not sure how ECT effects memory function though since stimulation is usually to cortex and should not involve direct stimulation of the hippocampus.
Orbz
Mar 19, 2007, 10:44 PM
Interestingly enough, someone was telling me the other day about how they withdrew from heroin using high doses of intravenous ketamine and temazepam whenever they were conscious enough to dose themselves in somebodies basement. They lasted four days (from what he can remember it was four days).
lucid_dream
Mar 19, 2007, 10:52 PM
intravenous ketamine and temazepam? That's an unusual mix. Would imagine that it would put you to sleep fast. For psychedelic effects, ketamine is usually administered IM, and only lasts 45 mins.
Trip like I do
Mar 20, 2007, 07:56 AM
Reading your posts also put me to sleep pretty fast!
Dbc
Mar 21, 2007, 02:49 AM
QUOTE(lucid_dream @ Mar 19, 2007, 06:11 PM)

DXM is definitely not the optimal NMDA antagonist to experiment around with. Also, see
Of course its not but we have to work with what tools we have sometimes. DXM's abuse potential is in the fact that it acts as a dopamine reuptake inhibitor. As a recreational experiance though i think most people view it as quite unfavorable.
It did its job decently i hear as far as eliminating the first two days of anxiety/stress of alprazolam withdrawal.
lucid_dream
Mar 21, 2007, 07:36 AM
Dbc, where did you hear that dopamine DXM is a DA reuptake inhibitor? To my knowledge, all NMDAR antagonists have abuse potential.
Dbc
Mar 21, 2007, 09:11 AM
QUOTE(lucid_dream @ Mar 21, 2007, 07:36 AM)

Dbc, where did you hear that dopamine DXM is a DA reuptake inhibitor? To my knowledge, all NMDAR antagonists have abuse potential.
I cant post links yet, so type dopamine reuptake dextromethorphan into google and you get many technical articles on it (ie not just wikipedia).
lucid_dream
Mar 21, 2007, 09:31 AM
the Wikipedia source points to
http://www.nhtsa.dot.gov/PEOPLE/injury/res...omethorphan.htm , which claims "It is proposed that dextromethorphan is a glutamate and NMDA antagonist, and blocks the dopamine reuptake site", but it does not cite any sources.
Running a Pubmed search for "dopamine reuptake dextromethorphan" yields nothing.
lcsglvr
Mar 28, 2007, 01:48 PM
QUOTE(lucid_dream @ Mar 20, 2007, 01:10 AM)

I don't know enough about how ECT effects brain function to say. NMDA antagonists usually activate limbic-related areas, and my guess would be that memory dysfunction is due to hippocampal dysfunction (perhaps through overactivation or activation of inhibitory circuitry). I'm not sure how ECT effects memory function though since stimulation is usually to cortex and should not involve direct stimulation of the hippocampus.
I am confused by what lucid_dream says. I am making assumptions that you are saying that NMDA antagonists have nothing to do with memory in the hippocampus? You are saying that it has more to do with faulty hippocampal functions rather than NMDA antagonists?
lucid_dream
Mar 28, 2007, 06:27 PM
what I meant was that NMDAR-antagonism-induced memory dysfunction is probably due to NMDAR-antagonism-induced hippocampal dysfunction (through NMDAR-antagonism-induced hippocampal overactivation or activation of hippocampal inhibitory circuitry).
lcsglvr
Mar 29, 2007, 07:52 AM
QUOTE(lucid_dream @ Mar 28, 2007, 10:27 PM)

what I meant was that NMDAR-antagonism-induced memory dysfunction is probably due to NMDAR-antagonism-induced hippocampal dysfunction (through NMDAR-antagonism-induced hippocampal overactivation or activation of hippocampal inhibitory circuitry).
That makes sense.
This is a "lo-fi" version of our main content. To view the full version with more information, formatting and images, please
click here.