http://www.ncbi.nlm....pubmed/10987845
Neurotoxic effects of amphetamines, which are linked
to increased extracellular glutamate levels, are associated
with the production of ROS and can be attenuated by
antioxidants (Cadet and Brannock, 1998; Yamamoto and
Zhu, 1998; Yamamoto et al., 1998). Our results suggest
that ROS are also involved in the more modest increases
in VTA glutamate efflux produced by doses of amphetamine that lack overt neurotoxicity. First, we observed
that amphetamine-induced glutamate efflux was prevented when D-phenylalanine, a trapping agent for hydroxyl radicals, was included in the microdialysis perfusion solution. Second, it was prevented when a different
trapping agent, PBN, was injected systemically prior to
amphetamine administration. Given these findings, it is
puzzling that amphetamine-induced increases in hydroxyl radical levels were not detected in D-phenylalanine trapping studies. It is possible that amphetamine did
increase hydroxyl radical levels, but we could not detect
the increase either because of insensitivity or because of
side reactions that occurred more rapidly than trapping
by D-phenylalanine. A recent study using a different
trapping procedure (salicylate hydroxylation) was able to
detect a significant increase in hydroxyl radical formation when 10 mM amphetamine was infused into rat
striatum by reverse dialysis (Wan et al., 2000). This
concentration of amphetamine is sufficient to increase
VTA glutamate efflux (Wolf and Xue, 1998).
Hm interesting, so phenylalanine actually traps amphetamine-induced glutamate efflux. That might help with one portion of Adderall's neurotoxicity? (although not all of it).
