Novelli A, Torreblanca A, Fernández-Sánchez M T
Departamento de Bioogia Funcional, Facultad de Medicina, Universidad de Oviedo, Spain.
Eur J Pharmacol. 1994 Aug 3;270(4):361-4. doi: 10.1016/0926-6917(94)90013-2.
Exposure of cultured cerebellar neurons to the putative metabotropic glutamate receptor antagonist L-2-amino-3-phosphonopropionate (L-AP3) for 24 h produced a neurotoxic effect which was prevented by the addition of the NMDA receptor antagonist (+)-10,11-dihydro-5-methyl-5-H-dibenzo-[a,d]-cyclohepten-5,1 0-imine hydrogen maleate (MK-801). MK-801 did also reduce neurotoxicity following 72 h exposure to L-AP3 neurotoxicity in the presence of MK-801 was antagonized by glutamate. Our results suggest that metabotropic glutamate receptors may play an important role in neuronal survival by controlling NMDA receptor-dependent as well as independent pathways.
将培养的小脑神经元暴露于假定的代谢型谷氨酸受体拮抗剂L-2-氨基-3-膦丙酸（L-AP3）24小时会产生神经毒性作用，而添加NMDA受体拮抗剂（+）-10,11-二氢-5-甲基-5-H-二苯并-[a,d]-环庚烯-5,10-亚胺氢马来酸盐（MK-801）可预防这种作用。MK-801在暴露于L-AP3 72小时后也能降低神经毒性，在存在MK-801的情况下，谷氨酸可拮抗L-AP3的神经毒性。我们的结果表明，代谢型谷氨酸受体可能通过控制NMDA受体依赖性和非依赖性途径在神经元存活中发挥重要作用。
