blocking amphetamine (adderall, dexedrine) tolerance

Im late to the party but I just wanted to point out a few things.
Contrary to popular belief, NMDA antagonists do not reset tolerance nor do they stave off tolerance. However, glutamate is definitely one of the key players in tolerance development.

A good place to start (which has been mentioned above) is calcium channel blockade. A perfect model for tolerance of all kinds of addictive drugs is benzodiazipne withdrawal. Just like amphetamine, prolonged use of benzos activates and facilitates strong currents through high voltage l-type calcium channels. When they are withdrawn, the calcium channel receptors stay in there aggressive state causing the worst hell imaginable. I have tried to taper xanax cold turkey twice and long term once and could not do it.

http://www.ncbi.nlm.nih.gov/pubmed/8707372

This article neatly simplifies the whole process of withdrawal and the complete attenuation of withdrawal symptoms with calcium channel blockers.

It appears that NMDA and AMPA receptors, which get a lot of attention, work downstream from the calcium channels. When you have excessive calcium channel currents this super activates the AMPA receptors which can be neurotoxic if the NMDA receptors do not down regulate. NMDA down regulation is a natural compensatory adaptation by your body to prevent against AMPA mediated excitotoxicity. So while blocking the NMDA receptors is in fact neuroprotective, it does not work back upstream and give feedback to shut down the ampa and calcium channel currents which mediate neurotransmitter sensitivity.

This excerpt is taken from the following article and backs the above statements:
"NMDAR antagonist administration (MK-801, 0.25 mg/kg intraperitoneally) had no effect on modifying increased glutamatergic strength or on withdrawal anxiety, whereas injection of an L-type voltage-gated calcium channel antagonist, nimodipine (10 mg/kg, intraperitoneally) averted AMPAR current enhancement and anxiety-like behavior, suggesting that these manifestations may be initiated by a voltage-gated calcium channel-dependent signal transduction pathway."

http://www.ncbi.nlm.nih.gov/pubmed/17762513

So back to amphetamines... They are an even stronger calcium channel stimulator, leading to even more profound downstream NMDA and AMPA adaptations...
So from a glutamate perspective there seem to be a couple options to help with tolerance:
1. A potent AMPA receptor antagonist (e.g. Topamax, others). These have a bad reputation of causing dumbing side effects so it may or may not be worth it.
2. High dose calcium channel blockers (e.g. Verapamil) which would cut the excitation near the source...
3. An NMDA AGONIST, yes, that is strange but pushing back against AMPA receptors with NMDA activation is known to stop AMPA mediated neurotoxicity (a perfect example of this is the strong, neuroprotective antidepressant Tianeptine which prevents excessive AMPA activation via an NMDA pathway). I can vouch for tianeptine.
4. 5htc-3 receptor antagonists (eg, agomelatine). No one seems to know why but blocking the 5ht3 receptor has potent glutamate modulating activity, case in point a schizophrenic man who withdrew from years of constant use of 100mg valium per day within a month without incident.
http://www.sciencedirect.com/science/article/pii/S0924933810709238

Finally I don't believe tolerance reversal is as simple as balancing out your glutamate system. Long term use of stimulants triggers a process known as dopamine subsensitivity where the d2 receptors in you're midbrain don't get impressed anymore with all the extra dopamine and start to metabolize it faster and downregulate. This is also what happens in the acute stages of schizophrenia. Typically, schizophrenics midbrain dopamine receptors are so subsensitive that dopamine barely reaches the higher level executive structures of the brain and those parts of the brain begin to deteriorate. They are the treated with all sorts of antipsychotics which, among other things, do the exact opposite of stims, they antagonize the dopamine receptors.

Luckily in the general population dopamine suisensitivity will not reach such astounding levels. Also, luckily, many of the the newer age antipsychotics (aripiprazole, brexipiprazole, quetiapine) are relatively weak antagonists and they only target the d2 receptors in the midbrain, allowing dopamine to flow freely around again.

So the last resort for tolerance reversal might be a short term treatment with a new age antipsychotic to resensitize those young dopamine receptors