Abstract
Direct protein interactions between the dopamine transporter and α-synuclein demonstrate that dopamine uptake function is modulated by α-synuclein. We report here that chronic cocaine abuse results in an increase in α-synuclein expression in the human striatum. Immunoblot analysis in the ventral putamen showed that α-synuclein protein was increased in striatal synaptosomes from cocaine users compared with age-matched drug-free controls. [3H]-Dopamine transporter uptake was increased in parallel with 2β-carbomethoxy-3β-(4-fluorophenyl)tropane binding to the dopamine transporter. The increase in α-synuclein protein was more marked in the ventromedial sectors of the striatum than in the dorsal caudate nucleus. These results demonstrate concomitant regulation of α-synuclein and dopamine transporter binding and function in human striatal synaptic terminals isolated from cocaine abusers. Overexpression of α-synuclein may play a role in cocaine-induced plasticity and regulation of dopamine synaptic tone.
| Original language | English |
|---|---|
| Pages (from-to) | 1489-1493 |
| Number of pages | 5 |
| Journal | NeuroReport |
| Volume | 16 |
| Issue number | 13 |
| DOIs | |
| State | Published - Sep 8 2005 |
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Keywords
- α-Synuclein
- Cocaine
- Dopamine uptake
- Human
- Postmortem
- Striatum
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Cocaine abuse elevates alpha-synuclein and dopamine transporter levels in the human striatum. / Qin, Yujing; Ouyang, Qinjie; Pablo, John; Mash, Deborah C.
In: NeuroReport, Vol. 16, No. 13, 08.09.2005, p. 1489-1493.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Cocaine abuse elevates alpha-synuclein and dopamine transporter levels in the human striatum
AU - Qin, Yujing
AU - Ouyang, Qinjie
AU - Pablo, John
AU - Mash, Deborah C
PY - 2005/9/8
Y1 - 2005/9/8
N2 - Direct protein interactions between the dopamine transporter and α-synuclein demonstrate that dopamine uptake function is modulated by α-synuclein. We report here that chronic cocaine abuse results in an increase in α-synuclein expression in the human striatum. Immunoblot analysis in the ventral putamen showed that α-synuclein protein was increased in striatal synaptosomes from cocaine users compared with age-matched drug-free controls. [3H]-Dopamine transporter uptake was increased in parallel with 2β-carbomethoxy-3β-(4-fluorophenyl)tropane binding to the dopamine transporter. The increase in α-synuclein protein was more marked in the ventromedial sectors of the striatum than in the dorsal caudate nucleus. These results demonstrate concomitant regulation of α-synuclein and dopamine transporter binding and function in human striatal synaptic terminals isolated from cocaine abusers. Overexpression of α-synuclein may play a role in cocaine-induced plasticity and regulation of dopamine synaptic tone.
AB - Direct protein interactions between the dopamine transporter and α-synuclein demonstrate that dopamine uptake function is modulated by α-synuclein. We report here that chronic cocaine abuse results in an increase in α-synuclein expression in the human striatum. Immunoblot analysis in the ventral putamen showed that α-synuclein protein was increased in striatal synaptosomes from cocaine users compared with age-matched drug-free controls. [3H]-Dopamine transporter uptake was increased in parallel with 2β-carbomethoxy-3β-(4-fluorophenyl)tropane binding to the dopamine transporter. The increase in α-synuclein protein was more marked in the ventromedial sectors of the striatum than in the dorsal caudate nucleus. These results demonstrate concomitant regulation of α-synuclein and dopamine transporter binding and function in human striatal synaptic terminals isolated from cocaine abusers. Overexpression of α-synuclein may play a role in cocaine-induced plasticity and regulation of dopamine synaptic tone.
KW - α-Synuclein
KW - Cocaine
KW - Dopamine uptake
KW - Human
KW - Postmortem
KW - Striatum
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UR - http://www.scopus.com/inward/citedby.url?scp=27744520577&partnerID=8YFLogxK
U2 - 10.1097/01.wnr.0000175617.39054.ba
DO - 10.1097/01.wnr.0000175617.39054.ba
M3 - Article
C2 - 16110277
AN - SCOPUS:27744520577
VL - 16
SP - 1489
EP - 1493
JO - NeuroReport
JF - NeuroReport
SN - 0959-4965
IS - 13
ER -