Dumuis A, Pin J P, Oomagari K, Sebben M, Bockaert J
Centre CNRS-INSERM de Pharmacologie-Endocrinologie, Montpellier, France.
Nature. 1990 Sep 13;347(6289):182-4. doi: 10.1038/347182a0.
Associative stimulation of N-methyl-D-aspartate (NMDA) receptors and quisqualate ionotropic receptors (Qi) induces long-term potentiation at particular glutamatergic synapses. Release of arachidonic acid as a result of stimulation of NMDA receptors has been proposed to play a part in the establishment of long-term potentiation. But long-term plasticity events at some other glutamatergic synapses do not involve activation of NMDA receptors. Here we report that in mature striatal neurons in primary cultures, quisqualate can release arachidonic acid by associatively activating both quisqualate metabotropic receptors coupled to phospholipase C (Qp) and Qi receptors. Independent activation of these two receptor types with specific agonists did not stimulate arachidonic acid release. These results support a role for the associative activation of Qp and Qi receptors in synaptic plasticity events, including long-term potentiation at particular synapses.
N-甲基-D-天冬氨酸（NMDA）受体与使君子氨酸离子型受体（Qi）的联合刺激可在特定的谷氨酸能突触处诱导长时程增强。有观点认为，NMDA受体受刺激后释放花生四烯酸在长时程增强的建立过程中发挥作用。但其他一些谷氨酸能突触处的长时程可塑性事件并不涉及NMDA受体的激活。在此我们报告，在原代培养的成熟纹状体神经元中，使君子氨酸可通过联合激活与磷脂酶C偶联的使君子氨酸代谢型受体（Qp）和Qi受体来释放花生四烯酸。用特异性激动剂分别激活这两种受体类型并不会刺激花生四烯酸的释放。这些结果支持了Qp和Qi受体的联合激活在突触可塑性事件（包括特定突触处的长时程增强）中所起的作用。
