Casado M, Dieudonné S, Ascher P
Laboratoire de Neurobiologie, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8544, Ecole Normale Supérieure, 46, rue d'Ulm, 75005 Paris, France.
Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11593-7. doi: 10.1073/pnas.200354297.
At the cerebellar synapse between the parallel fibers (PFs) and the Purkinje cells in the cerebellum, we have found that application of N-methyl-d-aspartate (NMDA) reversibly depresses the postsynaptic current. We present evidence that this depression involves NMDA receptors located on the presynaptic axons and requires that the NMDA application be combined with action potentials in the PFs. Unexpectedly, unlike other modulations mediated by presynaptic receptors, the NMDA-induced inhibition does not involve a depression of transmitter release. Because it is blocked by both nitric oxide synthase and soluble guanylate cyclase inhibitors, we propose that it involves a trans-synaptic mechanism in which NO released by the PFs decreases the glutamate sensitivity of the Purkinje cell.
在小脑的平行纤维(PFs)与浦肯野细胞之间的突触处,我们发现应用N-甲基-D-天冬氨酸(NMDA)可使突触后电流可逆性降低。我们提供的证据表明,这种抑制涉及位于突触前轴突上的NMDA受体,并且要求在PFs中NMDA的应用与动作电位相结合。出乎意料的是,与由突触前受体介导的其他调节不同,NMDA诱导的抑制并不涉及递质释放的减少。由于它被一氧化氮合酶和可溶性鸟苷酸环化酶抑制剂所阻断,我们提出它涉及一种跨突触机制,其中PFs释放的NO降低了浦肯野细胞对谷氨酸的敏感性。