<p>I have quite a bit of experience understanding the gluatmate system and in particular the NMDA receptor subtypes. NMDA receptors are a highly complex system, which effect neuro function in multipule and often opposite ways. NMDA receptors modulate virtually the location,composition and activity of almost all receptor types this is because they have heavily implicated in Long term potentiation and Long Term depression, which are terms to describe the strengthing and weakening of the interactions between neurons,The wikipedia articles have a good basic cover of this concept.</p>
<p>Nmda receptors are composed of multipule subunits that each have there own pore, THe main three are NR1A,NR2A NR2B. NR1a. NR1a is rather simple it is similar to an cAMP recetpor in that it only allows monovalent cations to enter, this means that this receptor is not involved with a change in LTP or LTD although it fasiclitates LTP and LTD via the other subunits, in other words it passes a signal, and in adults it plays an important role in keeping neural circiuts connected</p>
<p>The NR2(x)s play a different role, and that role depends whether or not there expressed on a synapse. For this discussion I shall limit talk to those NMDA receptors that are expressed on the syanpse.
The NR2A activity mediates quick actting and long term depression of the connection between neurons, From how I understand it thought is the turning off of particular connections on usually a short term basis. So the product of a thought and how it is expressed, is expressed by what in the system is still running after the said thought(this is grossly simplified). Therefore blocking the NR2a reduces the ability to hold a thought, and unfortunately the body doesnt upregulate NR2a activity in response to antagonists. Other systems do move them back and slowly they will reform. This is the heart of the Neurodamage of DMX and PCP.</p>
<p>NMDA</a> and AMPA Receptors</p>