期刊
JOURNAL OF NEUROCHEMISTRY
卷 105, 期 5, 页码 1668-1682出版社
WILEY
DOI: 10.1111/j.1471-4159.2008.05258.x
关键词
actin; depression; microtubule; norepinephrine transporter; Parkinson's disease; alpha-synuclein
资金
- NIMH NIH HHS [F31 MH76612, R01 MH075020, MH075020] Funding Source: Medline
One role of the actin cytoskeleton is to maintain the structural morphology and activity of the pre-synaptic terminal. We sought to determine if the actin cytoskeleton plays a role in regulating interactions between the norepinephrine transporter (NET) and alpha-Synuclein (alpha-Syn), two proteins expressed in the pre-synaptic terminal. In cells transfected with either 0.5 mu g/mL or 3 mu g/mL of alpha-Syn and 1 mu g/mL of NET DNA, treatment with cytochalasin D, an actin depolymerizing agent, caused a dose-dependent decrease and increase, respectively, in [H-3]-NE uptake. Protein interactions between NET, beta-actin, and alpha-Syn were modified, along with levels of surface transporters. Treatment of primary brainstem neurons and frontal cortex synaptosomes with cytochalasin D caused a 115% and 28% increase, respectively, in NET activity. Depolymerization of both actin and microtubules did not alter NET activity in cells with 0.5 mu g/mL alpha-Syn, but caused an increase in [H-3]-NE uptake in cells transfected with 3 mu g/mL of alpha-Syn and primary neurons. This is the first direct demonstration of NET activity being regulated via actin and modulated by interactions with alpha-Syn.
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