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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >AMPA receptor activation regulates the glutamate metabotropic receptor stimulated phosphatidylinositol turnover in human cerebral cortex slices.
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AMPA receptor activation regulates the glutamate metabotropic receptor stimulated phosphatidylinositol turnover in human cerebral cortex slices.

机译：AMPA受体激活调节人大脑皮质切片中谷氨酸代谢型受体刺激的磷脂酰肌醇的转换。

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摘要

The effect of excitatory amino acids (EAA) on phosphatidylinositol (PI) turnover in human cerebral cortical slices was investigated. Trans-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) increased inositol phosphate (IP) formation in the 1-1000 microM range. Quisqualic acid (QA) was maximally effective at 10-100 microM, showing an inverse correlation between concentration and effect in the 100-1000 microM range. The glutamate metabotropic receptor antagonist 2-amino-3-phosphonopropionic acid (AP3), the ionotropic non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the NMDA channel blocker dizolcipine (MK-801) failed to prevent the PI response to ACPD (1000 microM). However, CNQX (100 microM) modified the concentration-response curve of QA reducing the effect of QA 10 microM by approx. 50% and enhancing that of QA 1000 microM by 2-fold. In addition, CNQX (100 microM) together with MK-801 (100 microM) unmasked the ability of L-glutamate (L-GLU) 3000 microM to stimulate PI turnover. The effect of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) on the EAA-induced PI turnover was also studied. AMPA (0.1-1 microM) potentiated the response to submaximal (30 microM) ACPD and (1 microM) QA concentrations. However, higher AMPA concentrations (10 microM) failed to synergize with ACPD 30 microM and, in addition, inhibited the PI turnover maximally stimulated by QA 10 microM. These results further support the presence of the glutamate metabotropic receptor in the human neocortex. In addition, they show the occurrence of a concentration-related dual interaction between AMPA and glutamate metabotropic receptor activation in the IP formation in this brain area.
机译：研究了兴奋性氨基酸（EAA）对人大脑皮层切片中磷脂酰肌醇（PI）周转的影响。反式-1-氨基环戊烷-1,3-二羧酸（ACPD）在1-1000 microM范围内增加了肌醇磷酸酯（IP）的形成。异喹啉酸（QA）在10-100 microM时发挥最大作用，显示浓度与100-1000 microM范围内的效应呈负相关。谷氨酸代谢型受体拮抗剂2-氨基-3-膦酸丙酸（AP3），离子型非NMDA受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）和NMDA通道阻滞剂地佐辛（MK-801 ）未能阻止PI对ACPD（1000 microM）的响应。但是，CNQX（100 microM）修改了QA的浓度-响应曲线，从而使QA 10 microM的作用降低了约20％。 50％，并将QA 1000 microM的质量提高2倍。此外，CNQX（100 microM）与MK-801（100 microM）一起揭示了L-谷氨酸（L-GLU）3000 microM刺激PI转换的能力。还研究了α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）对EAA诱导的PI周转的影响。 AMPA（0.1-1 microM）增强了对最大（30 microM）ACPD和（1 microM）QA浓度的响应。但是，较高的AMPA浓度（10 microM）无法与ACPD 30 microM协同作用，此外，还抑制了由QA 10 microM最大程度刺激的PI转换。这些结果进一步支持了在人新皮层中谷氨酸代谢型受体的存在。此外，它们显示了在该大脑区域IP形成中，AMPA与谷氨酸代谢型受体激活之间存在浓度相关的双重相互作用。

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