^^ Quite low relative to the dose range. I usually take it daily for sleep at 300mg since I have reasons to avoid the usual addictive sleep aids but still needed a strong one.
For those methamp break days I usually only need 150mg since by that point your body is so drained and tired, this dose is enough to kill the amps and bring on sleep. Higher doses i found to strong causing an uncomfortable scary sensation of falling unconscious in a bad way and you tend to fight it out of fear.
The dose of seroquel isn't too bad -- sure 25 mg can knock someone out who doesn't take it regularly, but it's not going to be occupying barely any d2 receptors at that dose. It isn't until you get to close to about 300 mg (if you weigh approx. 160 lbs or so -- all assuming that the data Astra-Zeneca provides on this question based on rat brains is actually generalizable to humans) that more than 50% of d2 receptors are occupied, and even then not for terribly long. I've often wondered about this, as I take 70mg Vyvanse daily (occasionally I take a second one though I usually pay for it tolerance-wise until my next break) and 200 mg seroquel every evening. I've noticed that when I titrate down to 100 mg, I get a week or two of the Vyvanse working better than normal, but invariably that stops and also I tend to get depressed which leads me to raise my dose to 200 mg, which for whatever reason always pulls me out of a depression within a couple of days and restores the efficacy of the vyvanse.
So, given what I know, what I suspect, and what I've experienced, I think its certainly plausible that the seroquel + the good solid rest are doing something to attenuate the down-regulation of d2 receptors that presumably underlies amphetamine tolerance. But on the other hand, if this were true, we would probably expect to see much larger doses of seroquel in people not taking amphetamines to cause the up regulation of dopamine receptors, and we know that seroquel fortunately tends not to do that unless you take a really high dose for a really long time -- fortunately because up regulation of dopamine receptors => tardive dyskinesia as I understand it. Perhaps the fact that the receptors are already in flux because of the amphetamine makes a difference, but it sure would be nice to have actual evidence. Seroquel does lots of other stuff too -- perhaps the 5ht3 antagonism is relevant (studies have shown under certain conditions selective 5ht3 antagonists like ondansetron can reverse sensitization and tolerance to methamphetamine).
The last plausible mechanism, at least based on my personal experiences with the medicine, is that perhaps it is less about 'tolerance' per se than some sort of acute depression related to coming down / withdrawing. I don't know about recreational doses, but I sure know that when I'm depressed, I can take my regular dose of vyvanse and then lay in bed all day, but when I'm not depressed that same dose is very effective. So perhaps the seroquel-sleep pattern pushes back against some kind of pro-depression effect, and that's the reason the stimulant works better the next time you take it. Difficult not to speculate here, as many of the neurobiological factors that are relevant here are beyond the scope of current science.
So really, the only thing I can say with real confidence is that I think it is plausible that the seroquel is helping make your subsequent dose more effective despite not taking as long of a break. But maybe some others who have insight about some of what I discussed above might be able to definitely rule out some of the tentative theories/ideas...
