Zwartsen Anne, Olijhoek Michiel E, Westerink Remco H S, Hondebrink Laura
Neurotoxicology Research Group, Toxicology Division, Institute for Risk Assessment Sciences (IRAS), Faculty of Veterinary Medicine, Utrecht University, Utrecht, Netherlands.
Dutch Poisons Information Center (DPIC), University Medical Center Utrecht, Utrecht University, Utrecht, Netherlands.
Front Neurosci. 2020 Jan 29;14:9. doi: 10.3389/fnins.2020.00009. eCollection 2020.
Synthetic cathinones are the second largest class of new psychoactive substances (NPS) on the drug market. Despite the large number of different cathinones and their abundant use, hazard characterization is mainly limited to their potential to inhibit monoamine transporters. To expand the current hazard characterization, we first investigated the acute effects of several synthetic cathinones [4-methylethcathinone (4-MEC), 3-methylmethcathinone (3-MMC), 4-MMC, methylone, pentedrone, α-pyrrolidinovalerophenone (α-PVP), and 3,4-methylenedioxypyrovalerone (MDPV)] on human dopamine, norepinephrine, and serotonin reuptake transporters (hDAT, hNET, and hSERT), which were stably transfected in human embryonic kidney (HEK) 293 cells. Next, we examined effects on spontaneous neuronal activity in rat primary cortical cultures grown on microelectrode arrays (MEAs) as an integrated endpoint for neurotoxicity. Changes in neuronal activity were assessed after acute (30 min) and prolonged (4.5 h) exposure. Moreover, we investigated whether neuronal activity recovered after washout of the exposure (24 h after the start of the 5 h exposure). Low micromolar concentrations of synthetic cathinones inhibited monoamine uptake via hDAT and hNET, while higher cathinone concentrations were needed to inhibit uptake via hSERT. Comparable high concentrations were needed to inhibit spontaneous neuronal activity during acute (30 min) and prolonged (4.5 h) exposure. Notably, while the inhibition of neuronal activity was reversible at low concentrations, only partial recovery was seen following high, but non-cytotoxic, concentrations of synthetic cathinones. Synthetic cathinones with either a pyrrolidine moiety or long alkyl-tail carbon chain more potently inhibit monoamine uptake via hDAT and neuronal activity. Monoamine uptake via hNET was most potently inhibited by synthetic cathinones with a pyrrolidine moiety. The combination of integrated measurements (MEA recordings of neuronal activity) with single target assays (monoamine reuptake transporter inhibition) indicates inhibition of hDAT and hNET as the primary mode of action of these synthetic cathinones. Changes in neuronal activity, indicative for additional mechanisms, were observed at higher concentrations.
合成卡西酮是毒品市场上第二大类新型精神活性物质(NPS)。尽管卡西酮种类繁多且使用广泛,但其危害特征主要局限于抑制单胺转运体的潜力。为了扩展当前的危害特征描述,我们首先研究了几种合成卡西酮[4-甲基乙基卡西酮(4-MEC)、3-甲基甲基卡西酮(3-MMC)、4-MMC、甲酮、戊地酮、α-吡咯烷戊酮(α-PVP)和3,4-亚甲基二氧吡咯戊酮(MDPV)]对稳定转染于人类胚胎肾(HEK)293细胞中的人类多巴胺、去甲肾上腺素和5-羟色胺再摄取转运体(hDAT、hNET和hSERT)的急性影响。接下来,我们检测了对生长在微电极阵列(MEA)上的大鼠原代皮质培养物中自发神经元活动的影响,以此作为神经毒性的综合终点指标。在急性(30分钟)和延长(4.5小时)暴露后评估神经元活动的变化。此外,我们还研究了在暴露洗脱后(5小时暴露开始后24小时)神经元活动是否恢复。低微摩尔浓度的合成卡西酮通过hDAT和hNET抑制单胺摄取,而抑制hSERT摄取则需要更高的卡西酮浓度。在急性(30分钟)和延长(4.5小时)暴露期间,抑制自发神经元活动需要相当高的浓度。值得注意的是,虽然低浓度时神经元活动的抑制是可逆的,但在高浓度但无细胞毒性的合成卡西酮作用后,仅观察到部分恢复。含有吡咯烷部分或长烷基尾碳链的合成卡西酮更有效地通过hDAT抑制单胺摄取和抑制神经元活动。通过hNET的单胺摄取最容易被含有吡咯烷部分的合成卡西酮抑制。综合测量(神经元活动的MEA记录)与单一靶点检测(单胺再摄取转运体抑制)相结合表明,抑制hDAT和hNET是这些合成卡西酮的主要作用方式。在更高浓度下观察到了指示其他机制的神经元活动变化。