Hello everyone
Sad to say this is a very complex topic.. NMDA receptors are not just NMDA receptors.. there are various receptor isoforms of them and each of the above mentioned drugs i.e DXM, ketamine, PCP, ibogaine, all have varying affinities at different subunits in the different isoforms of the receptor(note: complicated).. Explained below.. first however I think addressing the study is very important..
First we must recognize the demographic, notably the study's funded statement: (quoted) "
This study had consents from patients and was approved by the ethical committee of Sun Yat-sen University, Guang Zhou, China". They used 21 patients and do claim to recognize that possible concomitant drug usage can possibly intensify the damage.. However these studies are very difficult to correctly manage as polysubstance abuse is critically correlated in many populations that abuse dissociative drugs.
I personally disagree with their methods as they actually provide a chart that attempts to correlate time of abuse with regions or areas of damage notably utilizing every addict in the study and not just ones that abused ketamine or had similar usage. The thing is they can do this- they can make figures, draw conclusions on their populace with their data, but everyone else must be careful to interpret their data as what it actually is, a study that shows hyperintensities in addicts that "MAY primarily have abused ketamine and MAY as well have abused many other drugs"...
Regardless, look at the wikipedia page for glutamate receptors
http://en.wikipedia.org/wiki/Glutamate_receptor
You will see the vast amounts of subunits that are recognized now that are metabotropic or ionotropic for different glutamate receptors.. no glutamate receptor is as simple as we believe..
Consider the NMDA receptor family now..
http://en.wikipedia.org/wiki/NMDA_receptor
"
The NMDA receptor forms a heterotetramer between two GluN1 and two GluN2 subunits (the subunits were previously denoted as NR1 and NR2), two obligatory NR1 subunits and two regionally localized NR2 subunits. A related gene family of NR3 A and B subunits have an inhibitory effect on receptor activity. Multiple receptor isoforms with distinct brain distributions and functional properties arise by selective splicing of the NR1 transcripts and differential expression of the NR2 subunits."
tldr; NMDA is not just 2(NR1)+2(NR2) it is now known to be 2(NRX1)+2(NRX2): In where NR1 and NR2 can be mutatable.
GLuN1 variants:
- NR1-1a, NR1-1b; [NR1-1a is the most abundantly expressed form.]
- NR1-2a, NR1-2b;
- NR1-3a, NR1-3b;
- NR1-4a, NR1-4b;
GluN2 variants are more complicated..read the page..Apparently this subunit is directly modified in an important manner during aging..
see the NR2B-NR2A developmental switch---> NR2A eventually outnumbers NR2B
http://en.wikipedia.org/wiki/NMDA_receptor
What makes the NMDA receptor so interesting is that despite the many isoforms the function is literally conserved(unlike serotonin receptors and their blatant subtypes) but we can only identify the changes now due to the ability to bind our man-made ligands, with some having notably high selectivity for binding to various subunits..
All i can say first hand is each of the examples presented originally above are not as simple as they appear and this idea I cannot even consider without seeing some affinity/binding tables for each of the compared drugs at least..
zedsdead
