Would 6-apb have any effect if I had ethyphenidate several hours earlier?

[lynx2051]

I have heard that dopamine re-uptake inhibitors cause releasing agent like 6-apb, aMT, MDMA to not have any effect if taken afterwards. I last dosed on Ethyphenidate at 13:00. I still feel some mild stimulation from it four hours later. If I took a 6-apb pill between 20:00-21:00 do you think it still wouldn't work?

 

[SNR]

It's true that DRI's will blunt the effects of DRA's. Like how MPH will block the effects of amphetamine. Ethylphenidate will block access to the dopamine transporter, so some releasing effects would be blunted (Some, as the EPH is probably wearing off a bit by now). However 6-APB (According to wikipedia) is also a monoamine reuptake inhibitor and a 5-HT2 agonist. So you will still have some effects from it.

 

[basement_shaman]

I was having a similar argument on another forum, regarding MDMA as and SSRA and SSRIs. Isn't it true that the SSRI would bind to the SERT that MDMA binds to, preventing it from performing the backwards transport of serotonin, effectively blunting the MDMA's effects?

 

[ebola?]

However 6-APB (According to wikipedia) is also a monoamine reuptake inhibitor and a 5-HT2 agonist.

All releasers are to some extent also reuptake inhibitors, so this doesn't tell us much. Also, notice the lack of proper citation on wikipedia: this is speculation.

ebola

 

[Amu]

All releasers are to some extent also reuptake inhibitors, so this doesn't tell us much. Also, notice the lack of proper citation on wikipedia: this is speculation.

ebola

It is due to the conformational changes the subtrate for the transporter causes, and of course post-treatment will have a weaker effect than pre-treatment, you would also need a transporter blocker with a fairly high affinity. All releasers being re-uptake inhibitors isn't really a counter issue, since they are blocking the inhibitors at low doses while the concentration of neurotransmitters is low, this is why d-amphetamine does not cause release of dopamine at low doses, then the same transporters blocked undergo reversal at high doses. I also believe the person's particular neuronal wiring also has an effect, for example if you had low dopamine D1 receptor density and did not have an unusually excessive amount of NET/DAT, then pre-administration might be have more numbing power on the releasing agent since there is already so few transporters that could possibly undergo phosphorylation, and the lower the doses of the two agents the less this effect will be.