http://www.ncbi.nlm.nih.gov/pubmed/9838055 "Dose-related effects of MK-801 on acute and chronic methylphenidate administration - MK-801 pretreatment blocked the progressive locomotor sensitization expected during repeated methylphenidate administration. These findings suggest that MK-801 may exert a long-lasting effect on learning and memory process that result in a blocking of the development of sensitization."
I'm sorry, can you explain why you think a releasing agent is functionally different than reuptake inhibitor in regards to how the dopamine is binding to the receptors and activating downstream pathways that regulate tolerance and sensitization? Sensitization to dopamine (no matter the source) will still depend upon long term potentiation and such.
http://www.ncbi.nlm.nih.gov/pubmed/23284812 - "
Methylphenidate enhances NMDA-receptor response in medial prefrontal cortex via sigma-1 receptor: a novel mechanism for methylphenidate action. - Together, the present study demonstrates for the first time that MPH facilitates NMDA-receptor mediated synaptic transmission via σ1 receptor, and such facilitation requires PLC/IP3/PKC signaling pathway. This novel mechanism possibly explains the underlying mechanism for
MPH induced addictive potential" - By addictive potential they mean sensitization
http://www.ncbi.nlm.nih.gov/pubmed/2671566 - ""Reverse tolerance" was produced in rats and mice by repeated exposure to either
cocaine (*comment -
lets ignore for a moment that cocaine might be a DAT inverse agonist) or amphetamine. The locomotorstimulant effect was studied in mice; stereotypy and convulsions in rats. MK-801,
the NMDA antagonist, blocked the development of "reverse tolerance" to all three effects. In contrast, haloperidol selectively blocked "reverse tolerance" to cocaine-induced stereotypy but not to convulsions.
The data suggest that the glutamate system participates in the mechanism of "reverse tolerance" to the dopaminergic effects of cocaine and amphetamine, as well as to the convulsant effect of cocaine." -- As in you would not want to block glutamate.
http://www.ncbi.nlm.nih.gov/pubmed/9560846 - "The role of excitatory amino acids in behavioral sensitization to psychomotor stimulants." - "To summarize, NMDA, AMPA metabotropic glutamate receptors all participate in the development of sensitization, while maintenance of the sensitized state involves alterations in neurochemical measures of EAA transmission as well as in the expression and sensitivity of AMPA and NMDA receptors." - Once again, glutamate is important in sensitization and you would not want to block it.
Opiates are a different matter.
Also, even though amitriptyline is a pretty weak dopamine antagonist why would we want to give him dopamine antagonists? It would be functionally the same as him taking a break from Concerta and losing his long term potentiation, anyways anticholinergics increase dopamine flow :3 I mean I agree with increasing NGF/BDNF though, which btw Jason I'm sorry I didn't mention this before you placed your order but you should definitely check out
Noopept, it increases some things that are basically like growth hormone for the brain apparently without much risk of tolerance, Noopept can be stacked with whatever if you can handle it. It can increase focus and is stimulating by itself as well.