Striatal dopamine nerve terminal markers in human, chronic methamphetamine users

被引:618
作者
Wilson, JM
Kalasinsky, KS
Levey, AI
Bergeron, C
Reiber, G
Anthony, RM
Schmunk, GA
Shannak, K
Haycock, JW
Kish, SJ
机构
[1] CLARKE INST PSYCHIAT,HUMAN NEUROCHEM PATHOL LAB,TORONTO,ON M5T 1R8,CANADA
[2] ARMED FORCES INST PATHOL,DIV FORENS TOXICOL,WASHINGTON,DC 20306
[3] EMORY UNIV,DEPT NEUROL,ATLANTA,GA 30322
[4] TORONTO GEN HOSP,DEPT PATHOL NEUROPATHOL,TORONTO,ON M5G 2C4,CANADA
[5] NO CALIF FORENS PATHOL,SACRAMENTO,CA 95825
[6] OFF BROWN CTY MED EXAMINER,GREEN BAY,WI 54305
[7] LOUISIANA STATE UNIV,MED CTR,DEPT BIOCHEM & MOLEC BIOL,NEW ORLEANS,LA 70119
关键词
D O I
10.1038/nm0696-699
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Methamphetamine is a drug that is significantly abused worldwide. Although long-lasting depletion of dopamine and other dopamine nerve terminal markers has been reported in striatum of nonhuman primates receiving very high doses of the psychostimuiant(1-3), no information is available for humans. We found reduced levels of three dopamine nerve terminal markers (dopamine, tyrosine hydroxylase and the dopamine transporter) in post-mortem striatum (nucleus accumbens, caudate, putamen) of chronic methamphetamine users. However, levels of DOPA decarboxylase and the vesicular monoamine transporter, known to be reduced in Parkinson's disease(4,5), were normal. This suggests that chronic exposure to methamphetamine does not cause permanent degeneration of striatal dopamine nerve terminals at the doses used by the young subjects in our study. However, the dopamine reduction might explain some of the dysphoric effects of the drug, whereas the decreased dopamine transporter could provide the basis for dose escalation occurring in some methamphetamine users.
引用
收藏
页码:699 / 703
页数:5
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