Opitz T, Reymann K G
Department of Neurophysiology, Institute of Neurobiology and Brain Research, Magdeburg, Germany.
Neuroreport. 1991 Aug;2(8):455-7. doi: 10.1097/00001756-199108000-00011.
The possible involvement of the metabotropic glutamate receptor in mechanisms of posthypoxic neuronal damage was investigated in an in-vitro model of mild hypoxia with the stereoselective antagonist L-2-amino-3-phosphonopropionate (L-AP3). When 300 microM L-AP3 was present during hypoxia the evoked field potentials (population EPSP and population spike in the CA1 region of the hippocampus) recovered to about 80-100% of baseline values. The recovery without drug treatment reached only 40-75%. The NMDA antagonist D,L-2-amino-5-phosphonovalerate (100 microM) was equally effective as L-AP3, whereas the less effective and less specific isomer D-AP3 (300 microM) did not show any protective effect. The results suggest that the activation of metabotropic glutamate receptors plays a role in hypoxic injury.
利用立体选择性拮抗剂L-2-氨基-3-膦丙酸（L-AP3），在轻度缺氧的体外模型中研究了代谢型谷氨酸受体在缺氧后神经元损伤机制中的可能作用。当缺氧期间存在300微摩尔L-AP3时，诱发的场电位（海马体CA1区群体兴奋性突触后电位和群体峰电位）恢复到基线值的约80-100%。未经药物治疗的恢复率仅达到40-75%。NMDA拮抗剂D,L-2-氨基-5-膦戊酸（100微摩尔）与L-AP3同样有效，而效果较差且特异性较低的异构体D-AP3（300微摩尔）未显示出任何保护作用。结果表明，代谢型谷氨酸受体的激活在缺氧损伤中起作用。
