Linden D J, Dickinson M H, Smeyne M, Connor J A
Department of Neurosciences, Roche Institute of Molecular Biology, Nutley, New Jersey 07110.
Neuron. 1991 Jul;7(1):81-9. doi: 10.1016/0896-6273(91)90076-c.
Cerebellar long-term depression (LTD) is a model of synaptic plasticity in which conjunctive stimulation of parallel fiber and climbing fiber inputs to a Purkinje neuron induces a persistent depression of the parallel fiber-Purkinje neuron synapse. We report that an analogous phenomenon may be elicited in the cultured mouse Purkinje neuron when iontophoretic glutamate application and depolarization of the Purkinje neurons are substituted for parallel fiber and climbing fiber stimulation, respectively. The induction of LTD in these cerebellar cultures requires activation of both ionotropic (AMPA) and metabotropic quisqualate receptors, together with depolarization in the presence of external Ca2+. This postsynaptic alteration is manifest as a depression of glutamate or AMPA currents, but not aspartate or NMDA currents. These results strengthen the contention that the expression of cerebellar LTD is at least in part postsynaptic and provide evidence that activation of both ionotropic and metabotropic quisqualate receptors are necessary for LTD induction.
小脑长期抑制（LTD）是一种突触可塑性模型，其中平行纤维和攀缘纤维对浦肯野神经元的联合刺激会导致平行纤维 - 浦肯野神经元突触的持续抑制。我们报告称，当分别用离子电渗法施加谷氨酸和浦肯野神经元去极化替代平行纤维和攀缘纤维刺激时，在培养的小鼠浦肯野神经元中可能引发类似现象。在这些小脑培养物中诱导LTD需要离子型（AMPA）和代谢型quisqualate受体的激活，以及在外部Ca2 +存在下的去极化。这种突触后改变表现为谷氨酸或AMPA电流的抑制，但不是天冬氨酸或NMDA电流的抑制。这些结果强化了小脑LTD的表达至少部分是突触后性的这一论点，并提供了证据表明离子型和代谢型quisqualate受体的激活对于LTD诱导都是必需的。
