http://jpet.aspetjournals.org/cgi/content/abstract/315/1/91
http://www.breggin.com/Newstimulants.pdf (search for neurotoxicity)
from the second file:
"AMPH (Dexedrine, Adderall) is another FDA-approved drug for treating behavioral problems in children.
Yet the existence of AMPH neurotoxicity has also been documented for more than thirty years and
the mechanism continues to be refined (Huang, Wan, Tseng, and Tung, 1997).
Wagner et al. (1980) found that treating rhesus monkeys with AMPH leads to a long-lasting loss of
dopamine and dopamine uptake sites (receptors). Juan, McCann, and Ricaurte (1997) confirmed that
AMPH produces a depletion of striatal dopamine that is measurable on autopsy of mice at 5 days and
2 weeks (the final experiment). The animals were administered 4 doses of 10 mg/kg spaced 2 hours apart.
Robinson and Kolb (1997) treated rats with AMPH twice a day for 5 days a week for a total of 5 weeks
with a dose that was gradually increased from 1 to 8 mg/kg. Thirty-eight days later, they found lasting
structural modifications in the nucleus accumbens and prefrontal cortex neurons, including increased
length of dendrites and density of their spines. In a microdialysis study, Weiss, Hechtman, Milroy, and
Perlman (1997) treated rats with AMPH (1.5 mg/kg injected twice a day for 14 days). Seven days after
withdrawal, the animals continued to show a reduced dopamine release in the ventral striatum in response
to stress.
Camp, DeJonghe, and Robinson (1997) administered a rising dose of AMPH (1 to 10 mg/kg over
10 days) to rats and then withdrew the animals for 1 to 30 days. Using in vivo microdialysis, they
found changes lasting 1 month in norepinephrine concentrations in the hippocampus as well as altered
responses to AMPH challenge. They concluded that AMPH produces biochemical adaptations that far
outlast the acute drug effects and may account for both transient and more persistent discontinuation
effects in humans.
Melega et al. (1997b) used PET in vervet monkeys to determine presynaptic striatal dopamine function
following the administration of AMPH with small acute doses. The animals were given two doses
of 2 mg/kg, 4 hours apart. These doses produced marked decreases in dopamine synthesis (25% at
10–12 weeks) with a 16% reduction in one AMPH-treated animal at 32 weeks. Biochemical analysis
showed decreased striatal dopamine concentrations of 55% at 10–12 weeks. They concluded that acute
AMPH doses produce long-lasting “neurotoxicity”. In another study using larger, more chronic doses (4–
18 mg/kg over 10 days), Melega, Raleigh, Stout, Huang, and Phelps (1997a) found a gradual recovery
from neurotoxicity in the striatum over a two-year period after termination of treatment.
Addressing the use of stimulants for the treatment of children, Ellinwood and Tong (1996) concluded:
“Drug levels in children on a mg/kg basis are sometimes as high as those reported to produce chronic
CNS changes in animal studies” (p. 14). Juan et al. (1997) warned that when psychostimulants are indicated
as in ADHD, “it would seem prudent to prescribe methylphenidate rather than AMPH, since
methylphenidate appears to lack the DA neurotoxic potential that has been well documented for amphetamine”
(p. 174).
AMPH, like M-AMPH, has been demonstrated to be irreversibly neurotoxic and, on this basis alone,
should not be prescribed for children."
the thing about amphetamine is that it seems to more exclusively cause neurotoxicity to dopaminergic terminals, rather than both that and serotonergic axons like methamphetamine or MDMA.
![:\](https://bluelight.org/xf/BL_Images/Orig_Emoji/wrygrin.gif "wry grin :\")