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Striatal dopamine nerve terminal markers in human, chronic methamphetamine users
J M Wilson1, K S Kalasinsky, A I Levey
1Human Neurochemical Pathology Laboratory, Clarke Institute of Psychiatry, Toronto, Ontario, Canada.
Nature Medicine
|June 1, 1996
Summary
Chronic methamphetamine use in humans reduced dopamine nerve terminal markers, but did not cause permanent degeneration. This may explain drug-induced dysphoria and dose escalation in users.
Area of Science:
- Neuroscience
- Neuropharmacology
- Addiction Research
Background:
- Methamphetamine abuse is a global health issue.
- Previous studies in nonhuman primates showed high-dose methamphetamine caused long-lasting dopamine depletion.
- Human data on long-term effects of methamphetamine on dopamine nerve terminals were lacking.
Purpose of the Study:
- To investigate the long-term effects of chronic methamphetamine use on dopamine nerve terminal markers in the human striatum.
- To compare methamphetamine's effects with those observed in Parkinson's disease.
Main Methods:
- Analysis of post-mortem striatal tissue (nucleus accumbens, caudate, putamen) from chronic methamphetamine users.
- Measurement of dopamine, tyrosine hydroxylase, dopamine transporter, DOPA decarboxylase, and vesicular monoamine transporter levels.
Main Results:
- Reduced levels of dopamine, tyrosine hydroxylase, and dopamine transporter were observed in chronic methamphetamine users.
- Levels of DOPA decarboxylase and vesicular monoamine transporter remained normal, unlike in Parkinson's disease.
- These findings suggest no permanent degeneration of striatal dopamine nerve terminals at the studied doses.
Conclusions:
- Chronic methamphetamine use in humans leads to reduced dopamine nerve terminal markers, but not permanent degeneration.
- Dopamine reduction may contribute to methamphetamine-induced dysphoria.
- Decreased dopamine transporter levels could underlie dose escalation in methamphetamine users.
