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海洋胍生物碱短裸甲藻毒素816通过谷氨酸受体诱导皮质神经元原代培养物中的钙内流和细胞毒性。

The Marine Guanidine Alkaloid Crambescidin 816 Induces Calcium Influx and Cytotoxicity in Primary Cultures of Cortical Neurons through Glutamate Receptors.

作者信息

Mendez Aida G, Juncal Andrea Boente, Silva Siguara B L, Thomas Olivier P, Martín Vázquez Víctor, Alfonso Amparo, Vieytes Mercedes R, Vale Carmen, Botana Luís M

机构信息

Departamento de Farmacología, Facultad de Veterinaria, Universidad de Santiago de Compostela , Lugo 27002, Spain.

Geoazur, UMR Université Nice Sophia Antipolis-CNRS-IRD-OCA , 06560 Valbonne, France.

出版信息

ACS Chem Neurosci. 2017 Jul 19;8(7):1609-1617. doi: 10.1021/acschemneuro.7b00096. Epub 2017 Apr 24.

Abstract

Crambescidin 816 is a guanidine alkaloid produced by the sponge Crambe crambe with known antitumoral activity. While the information describing the effects of this alkaloid in central neurons is scarce, Cramb816 is known to block voltage dependent calcium channels being selective for L-type channels. Moreover, Cramb816 reduced neuronal viability through an unknown mechanism. Here, we aimed to describe the toxic activity of Cramb816 in cortical neurons. Since calcium influx is considered the main mechanism responsible for neuronal cell death, the effects of Cramb816 in the cytosolic calcium concentration of cortical neurons were studied. The alkaloid decreased neuronal viability and induced a dose-dependent increase in cytosolic calcium that was also related to the presence of calcium in the extracellular media. The increase in calcium influx was age dependent, being higher in younger neurons. Moreover, this effect was prevented by glutamate receptor antagonists, which did not fully block the cytotoxic effect of Cramb816 after 24 h of treatment but completely prevented Cramb816 cytotoxicity after 10 min exposure. Therefore, the findings presented herein provide new insights into the cytotoxic effect of Cramb816 in cortical neurons.

摘要

克蓝比西定816是一种由海绵动物克蓝比海绵产生的胍生物碱,具有已知的抗肿瘤活性。虽然描述这种生物碱对中枢神经元作用的信息很少,但已知克蓝比816能阻断电压依赖性钙通道,对L型通道具有选择性。此外,克蓝比816通过未知机制降低神经元活力。在此,我们旨在描述克蓝比816在皮质神经元中的毒性活性。由于钙内流被认为是导致神经元细胞死亡的主要机制,因此研究了克蓝比816对皮质神经元胞质钙浓度的影响。该生物碱降低了神经元活力,并诱导胞质钙呈剂量依赖性增加,这也与细胞外培养基中钙的存在有关。钙内流的增加与年龄有关,在较年轻的神经元中更高。此外,谷氨酸受体拮抗剂可预防这种效应,在处理24小时后,谷氨酸受体拮抗剂不能完全阻断克蓝比816的细胞毒性作用,但在暴露10分钟后可完全预防克蓝比816的细胞毒性。因此,本文的研究结果为克蓝比816对皮质神经元的细胞毒性作用提供了新的见解。

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