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Neurotrophic effect of isoquinoline derivatives in primary cortical culture

机译：异喹啉衍生物在原代皮层培养中的神经营养作用

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摘要

Recent studies indicate that the N-methyl-D-aspartate (NMDA) antagonist, (+)-1-methyl-1-phenyl-1,2,3,4-tetrahydroisoquinoline hydrochloride (FR115427), enhanced neuronal survival in primary culture of cortical neurons from mouse embryos. In the present study isoquinoline derivatives were examined for the neurotrophic activity in primary culture of cortical neurons and were also examined for anti-NMDA activity. In spite of varying level of anti-NMDA activity, isoquinoline derivatives enhanced neuronal survival at the concentration of 10 #mu#M. To elucidate of the mechanisms of neurotrophic activity in primary cortical culture, nicardipine and flunarizine, known calcium channel blockers, were also tested. Neither nicardipine nor flunarizine showed neurotrophic activity up to the doses causing toxicity in cultured neurons. NBQX, an AMPA receptor antagonist, was also tested for neurotrophic activity. However no enhancement of neuronal survival was observed. These data suggest that one of the mechanisms to promote neuronal survival may depend on the structure of isoquinoline ring. Moreover neurotrophic activity observed in our culture systems might not relate on anti-NMDA activity, blockade of voltage dependent L-type calcium channels and antagonization of AMPA receptor.
机译：最近的研究表明，N-甲基-D-天冬氨酸（NMDA）拮抗剂（+）-1-甲基-1-苯基-1,2,3,4-四氢异喹啉盐酸盐（FR115427）增强了原代培养的神经元存活。小鼠胚胎的皮质神经元。在本研究中，检查了异喹啉衍生物在皮层神经元原代培养物中的神经营养活性，还检查了其抗NMDA活性。尽管抗NMDA活性水平不同，但异喹啉衍生物在10＃mu＃M的浓度下仍能提高神经元的存活率。为了阐明初级皮层培养中神经营养活性的机制，还对尼卡地平和氟硝利嗪（已知的钙通道阻滞剂）进行了测试。尼卡地平和氟硝利嗪均未显示神经营养活性，直至引起培养的神经元毒性的剂量为止。还测试了AMPA受体拮抗剂NBQX的神经营养活性。然而，没有观察到神经元存活的增强。这些数据表明，促进神经元存活的机制之一可能取决于异喹啉环的结构。此外，在我们的培养系统中观察到的神经营养活性可能与抗NMDA活性，电压依赖性L型钙通道的阻滞和AMPA受体的拮抗作用无关。

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