::: Sorry for the late reply - been busy.  Replying to the original post: text on this topic should normally go under a section titled "Toxicity" given its context; toxicity is intended as subsection under "Overdose" per the MOS:MED drug section + MOS:PHARM guidelines; however, in this particular article, either is fine IMO.  Long-term effects actually contains toxicity info at the moment anyway.  In any event, my original statement about it referring to high doses is really just referencing to the content+citations in the meth article's neurotoxicty section that covers the mechanism of indirect neurotoxicity as radical species and dopamine quinones (the autoxidation products). The astroglia mechanism of meth occurs through its binding at astroglia-localized TAAR1; these papers don't specify a dose, but indicate the relevant population is meth abusers, per the wording of both abstracts PMID 22591363 PMID 24950453. The glial cell NF-kB mechanism arises in response to these. 
 :::Regarding cross-species pharmacodynamic comparisons, data from an animal study, by itself, isn't applicable to humans for a variety of reasons - this topic is probably covered in animal testing, but I haven't looked.  For future reference relative to these compounds, the entire TAAR class has diverged across species over time to the point that each species has its own subset of TAARs genes. Moreover, TAAR1's sequence diverged across species as animals. Rat TAAR1 and human TAAR1 have very dissimilar sequences, and so there are a number of ligands which bind to one receptor but not the other, while the ligands that do have common binding activity often have a significantly different affinity and/or potency at the receptor.  E.g., see PMID 17218486 and  on a few amphetamine derivative affinities at TAAR1 across species.