• Juhyun Song, Byeong C Kim, Dai-Trang T Nguyen, Manikandan Samidurai, and Seong-Min Choi.
• Department of Biomedical Sciences, Center for Creative Biomedical Scientists at Chonnam National University, Gwangju 61469, South Korea. Electronic address: juhyunsong@chonnam.ac.kr.
• Neuroscience. 2017 Sep 1; 358: 336-348.

AbstractParkinson's disease (PD) is characterized by the formation of Lewy bodies (LBs) in dopaminergic neurons. α-Synuclein (α-syn), a major protein component of LBs, is known to regulate synaptic plasticity, with a crucial role in memory and motor function in the central nervous system. Levodopa (L-3,4-dihydroxyphenylalanine; also known as L-DOPA) is considered the most effective medication for controlling the symptoms of PD. However, it is unclear whether L-DOPA improves the neuropathology of PD. In the present study, we investigated the effect of L-DOPA on SH-SY5Y neuronal cells under α-syn-induced toxicity. We assessed the protein and mRNA levels of endoplasmic reticulum (ER) stress and cell death markers using western blot analysis and reverse transcription-PCR. Our data showed that L-DOPA could attenuate ER stress markers, including the levels of activating transcription factor 4 (ATF4), C/EBPhomologous protein expression (CHOP), immunoglobulin-heavy-chain-binding protein (BiP), sliced X-box-binding protein 1 (XBP-1), and reduce nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling through dopamine receptor D2 (DRD2) in SH-SY5Y neuronal cells under α-syn-induced toxicity. In conclusion, we suggest that L-DOPA may attenuate the neuropathology of PD by regulating signaling related to DRD2 in neuronal cells under α-syn-induced toxicity. Our study, therefore, indicates an additional role for L-DOPA in the treatment of PD.Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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